Evidence map›Paper›PMID 41099493›Full record

ArticleCancer medicine2025

A Transcriptome-Wide Association Study Identifies Candidate Susceptibility Loci and Genes for Lung Cancer Risk.

Tianying Zhao, Jiajun Shi, Yaohua Yang, Dan Zhou, Jie Ping, Shuai Xu, Lili Xu, Jie Wu, Xiao-Ou Shu, Ran Tao and 4 more

Abstract read
In one paragraph

Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Tianying ZhaoDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0002-0103-1867
Jiajun ShiDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0001-5194-0009
Yaohua YangSchool of Medicine, University of Virginia, Charlottesville, Virginia, USA.ORCID https://orcid.org/0000-0002-3815-7172
Dan ZhouVanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0002-5313-8164
Jie PingDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0001-9907-5819
Shuai XuDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0002-7798-5720
Lili XuDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA.ORCID https://orcid.org/0009-0008-2580-7026
Jie WuDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0003-2181-8971
Xiao-Ou ShuDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0002-0711-8314
Ran TaoVanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0002-1106-2923
Bingshan LiDepartment of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0003-2129-168X
Wei ZhengDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0003-1226-070X
Jirong LongDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0002-7433-9766
Qiuyin CaiDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt University School of Medicine, Nashville, Tennessee, USA.ORCID https://orcid.org/0000-0002-9384-5648

Funding

Identification of Genes and DNA Methylation Markers for Lung Cancer Risk by Integrating Multi-omics DataR01CA249863 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CAI, QIUYIN, LONG, JIRONG · 2021 to 2025
$3.4M
NCI NIH HHS R01 CA249863NCI NIH HHS R01CA249863NIH HHSODCDC CDC HHS
6 · The paper itself

Abstract

backgroundGenome-wide association studies (GWAS) have identified over 80 susceptibility loci for lung cancer risk. However, the genes underlying these associations remain largely unknown.

methodsWe conducted a large transcriptome-wide association study (TWAS) to identify lung cancer susceptibility genes. We leveraged gene expression data from lungs and 48 other tissue types and whole-genome sequencing data from up to 706 samples of European ancestry in the GTEx (version 8) to build lung-tissue and joint-tissue gene expression prediction models. These models were applied to GWAS data, including 29,266 lung cancer cases and 56,450 controls, to assess the associations of genetically predicted gene expression levels with lung cancer risk.

resultsA total of 8624 genes were successfully built for single-tissue models, and 11,341 genes for joint-tissue models (12,133 unique genes altogether). Among 40 genes whose expression levels were associated with the risk of lung cancer at a Bonferroni-corrected significance level, ZKSCAN4 was located more than 2 Mb away from the GWAS-identified variants linked to lung cancer. Among the remaining 39 genes within 2 Mb of GWAS-identified variants, seven genes were independent of these. Among 53 genes associated with the risk of lung cancer subtypes, 13 genes were beyond 2 Mb of GWAS-identified variants, and four genes were independent of the GWAS-identified variants within 2 Mb regions.

conclusionOur TWAS identified over 50 candidate susceptibility genes for lung cancer, providing new insights into lung cancer genetics.

Indexed as

Genetic Predisposition to DiseaseLung NeoplasmsTranscriptomeCase-Control StudiesFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGenome-Wide Association StudyHumansMalePolymorphism, Single Nucleotidegene expressionlung cancersusceptibility genestranscriptome‐wide association study

Identifiers

PMID41099493
PMCPMC12529646

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.