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首页> 外文期刊>Cancer epidemiology, biomarkers and prevention: A publication of the American Association for Cancer Research >Cigarette smoking and risk of Hodgkin lymphoma: a population-based case-control study.
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Cigarette smoking and risk of Hodgkin lymphoma: a population-based case-control study.

机译:吸烟与霍奇金淋巴瘤的风险:一项基于人群的病例对照研究。

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BACKGROUND: Studies have inconsistently reported an association between tobacco smoking and Hodgkin lymphoma (HL) risk. The conflicting finding may reflect etiologic heterogeneity between HL subtypes, warranting further characterization of the relationship. METHODS: We collected information on tobacco-smoking habits in 586 classic HL cases and 3,187 population controls in a Danish-Swedish case-control study. HL EBV status was established for 499 cases by standard techniques. Odds ratios (OR) for an association with cigarette smoking were calculated by logistic regression for HL overall and stratified by age, sex, major histology subtypes, and tumor EBV status, adjusting for known confounders. RESULTS: Compared with never smokers, current cigarette smokers were at an increased overall HL risk [adjusted OR, 1.57; 95% confidence interval (95% CI), 1.22-2.03]. The association was strongest for EBV-positive HL (adjusted OR, 2.36; 95% CI, 1.51-3.71), but also applied to EBV-negative HL (adjusted OR, 1.43; 95% CI, 1.05-1.97; P(homogeneity EBV-pos) versus P(homogeneity EBV-neg) = 0.04). The association did not vary appreciably by age, sex, or histologic subtype, the apparent EBV-related difference present in all strata. There was no evidence of a dose-response pattern, whether by age at smoking initiation, daily cigarette consumption, number of years smoking, or cumulative number of cigarettes smoked. Similar results were obtained in analyses using non-HL patients (n = 3,055) participating in the founding study as comparison group. CONCLUSION: The observed association between cigarette smoking and HL risk is consistent with previous findings and biologically credible. Although not easily dismissed as an artifact, the limited evidence of a dose-response pattern renders the overall evidence of causality weak.
机译:背景:研究不一致地报道了吸烟与霍奇金淋巴瘤(HL)风险之间的关联。矛盾的发现可能反映了HL亚型之间的病因异质性,从而保证了这种关系的进一步表征。方法:在丹麦-瑞典病例对照研究中,我们收集了586例经典HL病例和3,187例人群控制中吸烟习惯的信息。通过标准技术确定了499例HL EBV状态。与吸烟相关的赔率(OR)是通过整体HL的logistic回归计算的,并按年龄,性别,主要组织学亚型和肿瘤EBV状况进行分层,并调整已知混杂因素。结果:与从未吸烟者相比,当前吸烟者的整体HL风险升高[校正后OR为1.57; 95%置信区间(95%CI),1.22-2.03]。对于EBV阳性HL(校正后的OR,2.36; 95%CI,1.51-3.71)的关联最强,但也适用于EBV阴性HL(校正后的OR,1.43; 95%CI,1.05-1.97; P(均质EBV -pos)与P(均匀性EBV-neg = 0.04)。年龄,性别或组织学亚型之间的关联性没有明显变化,所有阶层中均存在明显的EBV相关差异。没有证据显示剂量反应模式,无论是开始吸烟时的年龄,每日吸烟量,吸烟年数或累计吸烟量。使用参与创建研究的非HL患者(n = 3,055)作为比较组,在分析中获得了相似的结果。结论:吸烟与HL危险之间的相关性与先前的发现一致,并且在生物学上是可信的。尽管不容易将其视为假象,但剂量反应模式的有限证据使得因果关系的总体证据微弱。

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