Non-Hodgkin Lymphoma, Body Mass Index, and Cytokine Polymorphisms: A Pooled Analysis from the InterLymph Consortium.
Non-Hodgkin Lymphoma, Body Mass Index, and Cytokine Polymorphisms: A Pooled Analysis from the InterLymph Consortium.
复制标题
DOI：
10.1158/1055-9965.epi-14-1355
复制
发表时间：
2015-07
期刊：
影响因子：
--
通讯作者：
Roman E
中科院分区：
文献类型：
--
作者：
Kane E;Skibola CF;Bracci PM;Cerhan JR;Costas L;Smedby KE;Holly EA;Maynadié M;Novak AJ;Lightfoot TJ;Ansell SM;Smith AG;Liebow M;Melbye M;Morton L;de Sanjosé S;Slager SL;Wang SS;Zhang Y;Zheng T;Roman E
过度肥胖与淋巴瘤发生有关，可能是由细胞因子产生增加介导的，引起慢性炎症状态。肥胖，细胞因子多态性和选定的成熟B细胞肿瘤之间的关系的报告。来自InterLymph联盟（1988-2008）的9项美国/欧洲研究的4979例病例和4752例对照的数据被汇总。对于弥漫性大B细胞淋巴瘤（DLBCL）、滤泡性淋巴瘤（FL）和慢性淋巴细胞白血病/小淋巴细胞淋巴瘤（CLL/SLL），（来自自我报告的身高和体重）和细胞因子IL 1A的12种多态性（rs1800587），IL1B（rs16944，rs1143627），IL1RN（rs454078），IL2（rs2069762），IL6（rs1800795，rs1800797），IL10使用非条件logistic回归研究了TNF（rs 1800890，rs 1800896），TNF（rs 1800629），LTA（rs 909253）和CARD 15（rs 2066847）。BMI-多态性相互作用效应采用相互作用引起的相对超额风险（RERI）进行估计。肥胖（BMI≥ 30 kg m−2）与DLBCL风险相关（OR=1.33，95%CI 1.02-1.73），TNF-308 GA +AA也是如此（OR=1.24，95%CI 1.07-1.44）。总之，肥胖和TNF-308 GA +AA使DLBCL风险增加近两倍，相对于正常体重和TNF-308 GG（OR=1.93 95%CI 1.27-2.94），RERI为0.41（95%CI − 0.05，0.84，P（交互作用）=0.13）。对于FL和CLL/SLL，未观察到与肥胖或TNF-308 GA +AA单独或联合相关。没有证据表明肥胖和其他多态性之间的相互作用。我们的研究结果表明，细胞因子多态性通常不与BMI相互作用，以增加淋巴瘤的风险，但肥胖和TNF-308 GA +AA可能相互作用，以增加DLBCL的风险。需要使用更好的肥胖测量方法的研究来进一步研究肥胖和TNF-308 G>A在淋巴瘤发病机制中的相互作用。
Excess adiposity has been associated with lymphomagenesis, possibly mediated by increased cytokine production causing a chronic inflammatory state. The relationship between obesity, cytokine polymorphisms and selected mature B-cell neoplasms is reported. Data on 4979 cases and 4752 controls from nine American/European studies from the InterLymph consortium (1988–2008) were pooled. For diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL) and chronic lymphocytic leukaemia/small lymphocytic lymphoma (CLL/SLL), joint associations of body mass index (from self-reported height and weight) and 12 polymorphisms in cytokines IL1A (rs1800587), IL1B (rs16944, rs1143627), IL1RN (rs454078), IL2 (rs2069762), IL6 (rs1800795, rs1800797), IL10 (rs1800890, rs1800896), TNF (rs1800629), LTA (rs909253), and CARD15 (rs2066847) were investigated using unconditional logistic regression. BMI-polymorphism interaction effects were estimated using the relative excess risk due to interaction (RERI). Obesity (BMI≥30kg m−2) was associated with DLBCL risk (OR=1.33, 95%CI 1.02–1.73), as was TNF-308GA+AA (OR=1.24, 95%CI 1.07–1.44). Together, being obese and TNF-308GA+AA increased DLBCL risk almost two-fold relative to those of normal weight and TNF-308GG (OR=1.93 95%CI 1.27–2.94), with a RERI of 0.41 (95%CI −0.05,0.84, P(interaction)=0.13). For FL and CLL/SLL, no associations with obesity or TNF-308GA+AA, either singly or jointly, were observed. No evidence of interactions between obesity and the other polymorphisms were detected. Our results suggest that cytokine polymorphisms do not generally interact with BMI to increase lymphoma risk but obesity and TNF-308GA+AA may interact to increase DLBCL risk. Studies using better measures of adiposity are needed to further investigate the interactions between obesity and TNF-308G>A in the pathogenesis of lymphoma.