Abstract
Background: The etiology of Hodgkin lymphoma (HL) remains incompletely characterized. Studies of the association between smoking and HL have yielded ambiguous results, possibly due to differences between HL subtypes.
Patients and methods: Through the InterLymph Consortium, 12 case–control studies regarding cigarette smoking and HL were identified. Pooled analyses on the association between smoking and HL stratified by tumor histology and
Epstein–Barr virus (EBV) status were conducted using random effects models adjusted for confounders. Analyses included 3335 HL cases and 14 278 controls.
Results: Overall, 54.5% of cases and 57.4% of controls were ever cigarette smokers. Compared with never smokers, ever smokers had an odds ratio (OR) of HL of 1.10 [95% confidence interval (CI) 1.01–1.21]. This increased risk reflected
associations with mixed cellularity cHL (OR = 1.60, 95% CI 1.29–1.99) and EBV-positive cHL (OR = 1.81, 95% CI 1.27–2.56) among current smokers, whereas risk of nodular sclerosis (OR = 1.09, 95% CI 0.90–1.32) and EBV-negative HL
(OR = 1.02, 95% CI 0.72–1.44) was not increased.
Conclusion: These results support the notion of etiologic heterogeneity between HL subtypes, highlighting the need for HL stratification in future studies. Even if not relevant to all subtypes, our study emphasizes that cigarette smoking should
be added to the few modifiable HL risk factors identified.
Key words: Hodgkin lymphoma, case–control, cigarette smoking, epidemiology, Epstein–Barr virus, individual patient data meta-analysis
Patients and methods: Through the InterLymph Consortium, 12 case–control studies regarding cigarette smoking and HL were identified. Pooled analyses on the association between smoking and HL stratified by tumor histology and
Epstein–Barr virus (EBV) status were conducted using random effects models adjusted for confounders. Analyses included 3335 HL cases and 14 278 controls.
Results: Overall, 54.5% of cases and 57.4% of controls were ever cigarette smokers. Compared with never smokers, ever smokers had an odds ratio (OR) of HL of 1.10 [95% confidence interval (CI) 1.01–1.21]. This increased risk reflected
associations with mixed cellularity cHL (OR = 1.60, 95% CI 1.29–1.99) and EBV-positive cHL (OR = 1.81, 95% CI 1.27–2.56) among current smokers, whereas risk of nodular sclerosis (OR = 1.09, 95% CI 0.90–1.32) and EBV-negative HL
(OR = 1.02, 95% CI 0.72–1.44) was not increased.
Conclusion: These results support the notion of etiologic heterogeneity between HL subtypes, highlighting the need for HL stratification in future studies. Even if not relevant to all subtypes, our study emphasizes that cigarette smoking should
be added to the few modifiable HL risk factors identified.
Key words: Hodgkin lymphoma, case–control, cigarette smoking, epidemiology, Epstein–Barr virus, individual patient data meta-analysis
Original language | English |
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Article number | mdt218 |
Pages (from-to) | 2245-2255 |
Journal | Annals of oncology |
Volume | 24 |
Issue number | 9 |
DOIs | |
Publication status | Published - 19 Jun 2013 |