Additive interaction between hepatitis B virus infection and tobacco smoking on the risk of gastric cancer in a Chinese population.

IF 3.1 2区医学 Q3 IMMUNOLOGY

Infectious Agents and Cancer Pub Date : 2025-03-20 DOI:10.1186/s13027-025-00648-0

Danjing Chen, Rong Yu, Yongfeng Cai, He Zhang, Yijun Jiang, Yunli Wu, Xian-E Peng

{"title":"Additive interaction between hepatitis B virus infection and tobacco smoking on the risk of gastric cancer in a Chinese population.","authors":"Danjing Chen, Rong Yu, Yongfeng Cai, He Zhang, Yijun Jiang, Yunli Wu, Xian-E Peng","doi":"10.1186/s13027-025-00648-0","DOIUrl":null,"url":null,"abstract":"Objective: Although hepatitis B virus (HBV) infection was regarded as a risk factor for liver cancer, the association of HBV infection with gastric cancer (GC) is unclear. In this study, we aim to assess the association of HBV infection with the risk of GC and explore the interaction between HBV infection and other risk factors.Methods: A case-control study was conducted and 409 GC cases and 1275 healthy controls were enrolled in Fujian province, China. Serum hepatitis B surface antigen (HBsAg) was measured and epidemiological data were collected. The association between HBV infection and GC risk was analyzed using logistic regression and meta-analysis method was employed to make estimates more conservative. Meanwhile, multiplicative and additive models were used to explore the interaction between HBV infection and other risk factors.Results: The prevalence of serum HBsAg positivity was 13.20% among GC cases and 6.20% among controls. Compared to HBsAg-negative subjects, the adjusted odds ratios (OR) for HBsAg positive were 3.30 [95% confidence interval (CI): (1.84-5.91)]. Compared to HBsAg-negative never smokers, the adjusted OR was 2.00 (95%CI: 1.19-3.34) for HBsAg-negative ever smokers,4.27 (95%CI: 1.97-9.26) for HBsAg-positive never smokers, and 4.73 (95%CI: 1.85-12.08) for HBsAg-positive ever smokers. These evidences indicated super-additive [API (95%CI): 0.78 (0.67-0.90), S (95%CI): 5.45 (3.26-9.08)] between HBV infection and tobacco smoking. No interaction between HBV infection and alcohol drinking was found on the risk of GC.Conclusions: HBV infection increased the risk of GC, and tobacco smoking and HBV infection may positively interact in the development of GC.","PeriodicalId":13568,"journal":{"name":"Infectious Agents and Cancer","volume":"20 1","pages":"19"},"PeriodicalIF":3.1000,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11927330/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infectious Agents and Cancer","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13027-025-00648-0","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Objective: Although hepatitis B virus (HBV) infection was regarded as a risk factor for liver cancer, the association of HBV infection with gastric cancer (GC) is unclear. In this study, we aim to assess the association of HBV infection with the risk of GC and explore the interaction between HBV infection and other risk factors.

Methods: A case-control study was conducted and 409 GC cases and 1275 healthy controls were enrolled in Fujian province, China. Serum hepatitis B surface antigen (HBsAg) was measured and epidemiological data were collected. The association between HBV infection and GC risk was analyzed using logistic regression and meta-analysis method was employed to make estimates more conservative. Meanwhile, multiplicative and additive models were used to explore the interaction between HBV infection and other risk factors.

Results: The prevalence of serum HBsAg positivity was 13.20% among GC cases and 6.20% among controls. Compared to HBsAg-negative subjects, the adjusted odds ratios (OR) for HBsAg positive were 3.30 [95% confidence interval (CI): (1.84-5.91)]. Compared to HBsAg-negative never smokers, the adjusted OR was 2.00 (95%CI: 1.19-3.34) for HBsAg-negative ever smokers,4.27 (95%CI: 1.97-9.26) for HBsAg-positive never smokers, and 4.73 (95%CI: 1.85-12.08) for HBsAg-positive ever smokers. These evidences indicated super-additive [API (95%CI): 0.78 (0.67-0.90), S (95%CI): 5.45 (3.26-9.08)] between HBV infection and tobacco smoking. No interaction between HBV infection and alcohol drinking was found on the risk of GC.

Conclusions: HBV infection increased the risk of GC, and tobacco smoking and HBV infection may positively interact in the development of GC.

查看原文本刊更多论文

求助全文

约1分钟内获得全文求助全文

来源期刊

Infectious Agents and Cancer ONCOLOGY-IMMUNOLOGY

CiteScore

5.80

自引率

2.70%

发文量

期刊介绍： Infectious Agents and Cancer is an open access, peer-reviewed online journal that encompasses all aspects of basic, clinical, epidemiological and translational research providing an insight into the association between chronic infections and cancer. The journal welcomes submissions in the pathogen-related cancer areas and other related topics, in particular: • HPV and anogenital cancers, as well as head and neck cancers; • EBV and Burkitt lymphoma; • HCV/HBV and hepatocellular carcinoma as well as lymphoproliferative diseases; • HHV8 and Kaposi sarcoma; • HTLV and leukemia; • Cancers in Low- and Middle-income countries. The link between infection and cancer has become well established over the past 50 years, and infection-associated cancer contribute up to 16% of cancers in developed countries and 33% in less developed countries. Preventive vaccines have been developed for only two cancer-causing viruses, highlighting both the opportunity to prevent infection-associated cancers by vaccination and the gaps that remain before vaccines can be developed for other cancer-causing agents. These gaps are due to incomplete understanding of the basic biology, natural history, epidemiology of many of the pathogens that cause cancer, the mechanisms they exploit to cause cancer, and how to interrupt progression to cancer in human populations. Early diagnosis or identification of lesions at high risk of progression represent the current most critical research area of the field supported by recent advances in genomics and proteomics technologies.