The association between human papillomavirus and lung cancer: A Mendelian randomization study

IF 2.6 4区医学 Q3 INFECTIOUS DISEASES Infection Genetics and Evolution Pub Date : 2024-07-24 DOI:10.1016/j.meegid.2024.105646

Zhongcheng Han, Ayixiamuguli Aizezi, Lili Ma, Ying Su, Lijuan Fan, Jiang Liu

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Abstract

Background

To investigate the causal relationship between human papillomavirus (HPV) and lung cancer, we conducted a study using the two-sample Mendelian randomization (TSMR).

Method

Data from genome-wide association studies (GWAS) were analyzed with HPV E7 Type 16 and HPV E7 Type 18 as exposure factors. The outcome variables included lung cancer, small cell lung cancer, adenocarcinoma and squamous cell lung cancer. Causality was estimated using inverse variance weighted (IVW), MR-Egger and weighted median methods. Heterogeneity testing, sensitivity analysis, and multiple validity analysis were also performed..

Results

The results showed that HPV E7 Type 16 infection was associated with a higher risk of squamous cell lung cancer (OR = 7.69; 95% CI:1.98–29.85; p = 0.0149). HPV E7 Type 18 infection significantly increased the risk of lung adenocarcinoma (OR = 0.71; 95% CI: 0.38–1.31; p = 0.0079) and lung cancer (OR = 7.69; 95% CI:1.98–29.85; p = 0.0292). No significant causal relationship was found between HPV E7 Type 16 and lung adenocarcinoma, lung cancer, or small cell lung carcinoma, and between HPV E7 Type 18 and squamous cell lung cancer or small cell lung carcinoma.

Conclusions

This study has revealed a causal relationship between HPV and lung cancers. Our findings provide valuable insights for further mechanistic and clinical studies on HPV-mediated cancer.

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人类乳头瘤病毒与肺癌的关系：孟德尔随机研究

背景：为了研究人类乳头瘤病毒（HPV）与肺癌之间的因果关系，我们采用双样本孟德尔随机法（TSMR）进行了研究：为了研究人类乳头瘤病毒（HPV）与肺癌之间的因果关系，我们采用双样本孟德尔随机法（TSMR）进行了一项研究：方法：以 HPV E7 16 型和 HPV E7 18 型为暴露因子，对全基因组关联研究（GWAS）的数据进行分析。结果变量包括肺癌、小细胞肺癌、腺癌和鳞状细胞肺癌。因果关系采用反方差加权法（IVW）、MR-Egger 法和加权中值法进行估计。此外，还进行了异质性测试、敏感性分析和多重有效性分析：结果显示，HPV E7 16 型感染与鳞状细胞肺癌的高风险相关（OR = 7.69; 95% CI:1.98-29.85; p = 0.0149）。HPV E7 18型感染会显著增加肺腺癌（OR = 0.71；95% CI：0.38-1.31；p = 0.0079）和肺癌（OR = 7.69；95% CI：1.98-29.85；p = 0.0292）的风险。在HPV E7 16型与肺腺癌、肺癌或小细胞肺癌之间，以及HPV E7 18型与鳞状细胞肺癌或小细胞肺癌之间，均未发现明显的因果关系：本研究揭示了 HPV 与肺癌之间的因果关系。结论：这项研究揭示了人乳头瘤病毒与肺癌之间的因果关系，我们的发现为进一步开展人乳头瘤病毒介导癌症的机理和临床研究提供了宝贵的见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Infection Genetics and Evolution 医学-传染病学

CiteScore

8.40

自引率

0.00%

发文量

215

审稿时长

82 days

期刊介绍： (aka Journal of Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases -- MEEGID) Infectious diseases constitute one of the main challenges to medical science in the coming century. The impressive development of molecular megatechnologies and of bioinformatics have greatly increased our knowledge of the evolution, transmission and pathogenicity of infectious diseases. Research has shown that host susceptibility to many infectious diseases has a genetic basis. Furthermore, much is now known on the molecular epidemiology, evolution and virulence of pathogenic agents, as well as their resistance to drugs, vaccines, and antibiotics. Equally, research on the genetics of disease vectors has greatly improved our understanding of their systematics, has increased our capacity to identify target populations for control or intervention, and has provided detailed information on the mechanisms of insecticide resistance. However, the genetics and evolutionary biology of hosts, pathogens and vectors have tended to develop as three separate fields of research. This artificial compartmentalisation is of concern due to our growing appreciation of the strong co-evolutionary interactions among hosts, pathogens and vectors. Infection, Genetics and Evolution and its companion congress [MEEGID](http://www.meegidconference.com/) (for Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases) are the main forum acting for the cross-fertilization between evolutionary science and biomedical research on infectious diseases. Infection, Genetics and Evolution is the only journal that welcomes articles dealing with the genetics and evolutionary biology of hosts, pathogens and vectors, and coevolution processes among them in relation to infection and disease manifestation. All infectious models enter the scope of the journal, including pathogens of humans, animals and plants, either parasites, fungi, bacteria, viruses or prions. The journal welcomes articles dealing with genetics, population genetics, genomics, postgenomics, gene expression, evolutionary biology, population dynamics, mathematical modeling and bioinformatics. We also provide many author benefits, such as free PDFs, a liberal copyright policy, special discounts on Elsevier publications and much more. Please click here for more information on our author services .