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Docosapentaenoic acid and lung cancer risk: A Mendelian randomization study.

ABSTRACT: BACKGROUND:Observational studies have shown that excessive dietary fat may be associated with lung carcinogenesis. However, findings from previous studies are inconsistent and it remains unclear whether docosapentaenoic acid (DPA), a kind of polyunsaturated fatty acid, is linked to the risk of lung cancer. The aim of this study is to investigate the causal effect of DPA on lung cancer with Mendelian randomization (MR) method. METHODS:With a two-sample MR approach, we analyzed the summary data from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE, 8866 individuals of European ancestry) Consortium and International Lung Cancer Consortium (ILCCO, 11 348 lung cancer cases and 15 861 controls; European ancestry) to assess the possible causal relationship of DPA on the risk of lung cancer. RESULTS:Our results indicated that genetically predicted higher DPA level has a positive association with lung cancer, where 1% higher DPA was associated with a 2.01-fold risk of lung cancer (odds ratio [OR]: 2.01, 95% CI = 1.34-3.01; P = 7.40 × 10-4 ). Additionally, lung cancer was not a causal factor for DPA. The results of MR-Egger regression analysis showed that there was no evidence for the presence of directional horizontal pleiotropy. CONCLUSIONS:Genetically elevated DPA is positively associated with risk of lung cancer, and more work is needed to investigate the potential mechanisms.

SUBMITTER: Liu J

PROVIDER: S-EPMC6488117 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Docosapentaenoic acid and lung cancer risk: A Mendelian randomization study.

Liu Jiaqing J Zhou Huaqiang H Zhang Yaxiong Y Huang Yan Y Fang Wenfeng W Yang Yunpeng Y Hong Shaodong S Chen Gang G Zhao Shen S Chen Xi X Zhang Zhonghan Z Shen Jiayi J Xian Wei W Zhan Jianhua J Zhao Yuanyuan Y Hou Xue X Ma Yuxiang Y Zhou Ting T Zhao Hongyun H Zhang Li L

Cancer medicine 20190211 4

<h4>Background</h4>Observational studies have shown that excessive dietary fat may be associated with lung carcinogenesis. However, findings from previous studies are inconsistent and it remains unclear whether docosapentaenoic acid (DPA), a kind of polyunsaturated fatty acid, is linked to the risk of lung cancer. The aim of this study is to investigate the causal effect of DPA on lung cancer with Mendelian randomization (MR) method.<h4>Methods</h4>With a two-sample MR approach, we analyzed the ...[more]

PMID: 30741477

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Project description:BackgroundLung cancer is the major cause of mortality in tumor patients. While its incidence rate has recently declined, it is still far from satisfactory and its potential modifiable risk factors should be explored.MethodsWe performed a two-sample Mendelian randomization (MR) study to investigate the causal relationship between potentially modifiable risk factors (namely smoking behavior, alcohol intake, anthropometric traits, blood pressure, lipidemic traits, glycemic traits, and fasting insulin) and lung cancer. Besides, a bi-directional MR analysis was carried out to disentangle the complex relationship between different risk factors. Inverse-variance weighted (IVW) was utilized to combine the estimation for each SNP. Cochrane's Q value was used to evaluate heterogeneity and two methods, including MR-Egger intercept and MR-PRESSO, were adopted to detect horizontal pleiotropy.ResultsThree kinds of smoking behavior were all causally associated with lung cancer. Overall, smokers were more likely to suffer from lung cancer compared with non-smokers (OR = 2.58 [1.95, 3.40], p-value = 2.07 x 10-11), and quitting smoking could reduce the risk (OR = 4.29[2.60, 7.07], p-value = 1.23 x 10-8). Furthermore, we found a dose-response relationship between the number of cigarettes and lung cancer (OR = 6.10 [5.35, 6.96], p-value = 4.43x10-161). Lower HDL cholesterol could marginally increase the risk of lung cancer, but become insignificant after Bonferroni correction (OR = 0.82 [0.68, 1.00], p-value = 0.045). In addition, we noted no direct causal relationship between other risk factors and lung cancer. Neither heterogeneity nor pleiotropy was observed in this study. However, when treating the smoking behavior as the outcome, we found the increased BMI could elevate the number of cigarettes per day (beta = 0.139[0.104, 0.175], p-value = 1.99x10-14) and a similar effect was observed for the waist circumference and hip circumference. Additionally, the elevation of SBP could also marginally increase the number of cigarettes per day (beta = 0.001 [0.0002, 0.002], p-value = 0.018).ConclusionSmoking behavior might be the most direct and effective modifiable way to reduce the risk of lung cancer. Meanwhile, smoking behavior can be affected by other risk factors, especially obesity.

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Docosapentaenoic acid and lung cancer risk: A Mendelian randomization study.

Publications

Docosapentaenoic acid and lung cancer risk: A Mendelian randomization study.

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