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Cytokine signaling pathway polymorphisms and AIDS-related non-Hodgkin lymphoma risk in the multicenter AIDS cohort study

Wong, Hui-Leea; Breen, Elizabeth Cb; Pfeiffer, Ruth Ma; Aissani, Brahimc; Martinson, Jeremy Jd; Margolick, Joseph Be; Kaslow, Richard Ac; Jacobson, Lisa Pe; Ambinder, Richard Fe; Chanock, Stephena; Martínez-Maza, Otonielb; Rabkin, Charles Sa

Erratum

The authors would like to correct an error published in Discussion, Sentence 14 of issue 7 of AIDS [1].

The sentence originally published:

“Interestingly, while the rs1800872_A allele, that correlates to higher IL10 production is associated with decreased risk for AIDS-NHL((12) and current study), the rs1800872_A allele however has been previously associated with faster AIDS progression(11).”

Should be changed to:

“Interestingly, while the rs1800872_A allele, that correlates to lower IL10 production is associated with decreased risk for AIDS-NHL((12) and current study), the rs1800872_A allele however has been previously associated with faster AIDS progression(11).”

AIDS. 24(12):1973, July 31, 2010.

doi: 10.1097/QAD.0b013e328332d5b1
Epidemiology and Social

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.

aNational Cancer Institute, Rockville, Maryland, USA

bDavid Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA

cUniversity of Alabama at Birmingham, Birmingham, Alabama, USA

dUniversity of Pittsburgh, Pittsburgh, Pennsylvania, USA

eJohns Hopkins University, Baltimore, Maryland, USA.

Received 23 April, 2009

Revised 2 September, 2009

Accepted 9 September, 2009

Correspondence to Hui-Lee Wong, MSc, PhD, Division of Epidemiology, Office of Surveillance and Biometrics, Center for Devices and Radiological Health, FDA WO66-4561, 10903 New Hampshire Av. Silver Spring, MD 20993-0002, USA. Tel: +1 301 796 6234; fax: +1 301 847 8140; e-mail: huilee.wong@fda.hhs.gov

© 2010 Lippincott Williams & Wilkins, Inc.