File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Tuberculosis infection and lung adenocarcinoma: Mendelian randomization and pathway analysis of genome-wide association study data from never-smoking Asian women

TitleTuberculosis infection and lung adenocarcinoma: Mendelian randomization and pathway analysis of genome-wide association study data from never-smoking Asian women
Authors
KeywordsLung adenocarcinoma
Lung cancer
Mendelian randomization
Pathway analysis
Tuberculosis
Issue Date2020
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ygeno
Citation
Genomics, 2020, v. 112 n. 2, p. 1223-1232 How to Cite?
AbstractWe investigated whether genetic susceptibility to tuberculosis (TB) influences lung adenocarcinoma development among never-smokers using TB genome-wide association study (GWAS) results within the Female Lung Cancer Consortium in Asia. Pathway analysis with the adaptive rank truncated product method was used to assess the association between a TB-related gene-set and lung adenocarcinoma using GWAS data from 5512 lung adenocarcinoma cases and 6277 controls. The gene-set consisted of 31 genes containing known/suggestive associations with genetic variants from previous TB-GWAS. Subsequently, we followed-up with Mendelian Randomization to evaluate the association between TB and lung adenocarcinoma using three genome-wide significant variants from previous TB-GWAS in East Asians. The TB-related gene-set was associated with lung adenocarcinoma (p = 0.016). Additionally, the Mendelian Randomization showed an association between TB and lung adenocarcinoma (OR = 1.31, 95% CI: 1.03, 1.66, p = 0.027). Our findings support TB as a causal risk factor for lung cancer development among never-smoking Asian women. Copyright © 2019. Published by Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/281186
ISSN
2017 Impact Factor: 2.91
2015 SCImago Journal Rankings: 1.281
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorWong, JYY-
dc.contributor.authorZhanga, H-
dc.contributor.authorHsiung, CA-
dc.contributor.authorXu, J-
dc.date.accessioned2020-03-09T09:51:20Z-
dc.date.available2020-03-09T09:51:20Z-
dc.date.issued2020-
dc.identifier.citationGenomics, 2020, v. 112 n. 2, p. 1223-1232-
dc.identifier.issn0888-7543-
dc.identifier.urihttp://hdl.handle.net/10722/281186-
dc.description.abstractWe investigated whether genetic susceptibility to tuberculosis (TB) influences lung adenocarcinoma development among never-smokers using TB genome-wide association study (GWAS) results within the Female Lung Cancer Consortium in Asia. Pathway analysis with the adaptive rank truncated product method was used to assess the association between a TB-related gene-set and lung adenocarcinoma using GWAS data from 5512 lung adenocarcinoma cases and 6277 controls. The gene-set consisted of 31 genes containing known/suggestive associations with genetic variants from previous TB-GWAS. Subsequently, we followed-up with Mendelian Randomization to evaluate the association between TB and lung adenocarcinoma using three genome-wide significant variants from previous TB-GWAS in East Asians. The TB-related gene-set was associated with lung adenocarcinoma (p = 0.016). Additionally, the Mendelian Randomization showed an association between TB and lung adenocarcinoma (OR = 1.31, 95% CI: 1.03, 1.66, p = 0.027). Our findings support TB as a causal risk factor for lung cancer development among never-smoking Asian women. Copyright © 2019. Published by Elsevier Inc.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ygeno-
dc.relation.ispartofGenomics-
dc.subjectLung adenocarcinoma-
dc.subjectLung cancer-
dc.subjectMendelian randomization-
dc.subjectPathway analysis-
dc.subjectTuberculosis-
dc.titleTuberculosis infection and lung adenocarcinoma: Mendelian randomization and pathway analysis of genome-wide association study data from never-smoking Asian women-
dc.typeArticle-
dc.identifier.emailXu, J: xusunjun@hku.hk-
dc.description.naturelink_to_OA_fulltext-
dc.description.natureeid_2-s2.0-85068966697-
dc.identifier.doi10.1016/j.ygeno.2019.07.008-
dc.identifier.pmid31306748-
dc.identifier.pmcidPMC6954985-
dc.identifier.scopuseid_2-s2.0-85068966697-
dc.identifier.hkuros309319-
dc.identifier.volume112-
dc.identifier.issue2-
dc.identifier.spage1223-
dc.identifier.epage1232-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats