TY - JOUR
T1 - Exposure to UV radiation and risk of Hodgkin lymphoma
T2 - A pooled analysis
AU - Monnereau, Alain
AU - Glaser, Sally L.
AU - Schupp, Clayton W.
AU - Smedby, Karin Ekström
AU - De Sanjosé, Silvia
AU - Kane, Eleanor
AU - Melbye, Mads
AU - Forétova, Lenka
AU - Maynadié, Marc
AU - Staines, Anthony
AU - Becker, Nikolaus
AU - Nieters, Alexandra
AU - Brennan, Paul
AU - Boffetta, Paolo
AU - Cocco, Pierluigi
AU - Glimelius, Ingrid
AU - Clavel, Jacqueline
AU - Hjalgrim, Henrik
AU - Chang, Ellen T.
PY - 2013/11/14
Y1 - 2013/11/14
N2 - Ultraviolet radiation (UVR) exposure has been inversely associated with Hodgkin lymphoma (HL) risk, but only inconsistently, only in a few studies, and without attention to HL heterogeneity. We conducted a pooled analysis of HL risk focusing on type and timing of UVR exposure and on disease subtypes by age, histology, and tumor-cell Epstein-Barr virus (EBV) status. Four case-control studies contributed 1320HLcasesand 6381 controls. We estimated lifetime, adulthood, and childhood UVR exposure and history of sunburn and sunlamp use. We used 2-stage estimation with mixed-effects models and weighted pooled effect estimates by inverse marginal variances. We observed statistically significant inverse associations with HL risk for UVR exposures during childhood and adulthood, sunburn history, and sunlamp use, but we found no significant doseresponse relationships. Risks were significant only for EBV-positive HL (pooled odds ratio, 0.56; 95% confidence interval, 0.35 to 0.91 for the highest overall UVR exposure category), with a significant linear trend for overall exposure (P 5.03). Pooled relative risk estimates were not heterogeneous across studies. Increased UVR exposure may protect against HL, particularly EBV-positive HL. Plausible mechanisms involving UVR induction of regulatory T cells or the cellular DNA damage response suggest opportunities for new prevention targets.
AB - Ultraviolet radiation (UVR) exposure has been inversely associated with Hodgkin lymphoma (HL) risk, but only inconsistently, only in a few studies, and without attention to HL heterogeneity. We conducted a pooled analysis of HL risk focusing on type and timing of UVR exposure and on disease subtypes by age, histology, and tumor-cell Epstein-Barr virus (EBV) status. Four case-control studies contributed 1320HLcasesand 6381 controls. We estimated lifetime, adulthood, and childhood UVR exposure and history of sunburn and sunlamp use. We used 2-stage estimation with mixed-effects models and weighted pooled effect estimates by inverse marginal variances. We observed statistically significant inverse associations with HL risk for UVR exposures during childhood and adulthood, sunburn history, and sunlamp use, but we found no significant doseresponse relationships. Risks were significant only for EBV-positive HL (pooled odds ratio, 0.56; 95% confidence interval, 0.35 to 0.91 for the highest overall UVR exposure category), with a significant linear trend for overall exposure (P 5.03). Pooled relative risk estimates were not heterogeneous across studies. Increased UVR exposure may protect against HL, particularly EBV-positive HL. Plausible mechanisms involving UVR induction of regulatory T cells or the cellular DNA damage response suggest opportunities for new prevention targets.
UR - http://www.scopus.com/inward/record.url?scp=84888216734&partnerID=8YFLogxK
U2 - 10.1182/blood-2013-04-497586
DO - 10.1182/blood-2013-04-497586
M3 - Journal article
C2 - 24016459
AN - SCOPUS:84888216734
SN - 0006-4971
VL - 122
SP - 3492
EP - 3499
JO - Blood
JF - Blood
IS - 20
ER -