Faculty, Staff and Student Publications

Language

English

Publication Date

10-1-2025

Journal

British Journal of Cancer

DOI

10.1038/s41416-025-03141-y

PMID

40775447

PMCID

PMC12449480

PubMedCentral® Posted Date

8-7-2025

PubMedCentral® Full Text Version

Post-print

Abstract

Background: Integrating genome-wide association study (GWAS) and transcriptomic datasets can identify mediators for genetic risk of cancer. Traditional methods often are insufficient as they rely on total gene expression measures and overlook alternative splicing, which generates different transcript-isoforms with potentially distinct effects.

Methods: We integrate multi-tissue isoform expression data from the Genotype Tissue-Expression Project with GWAS summary statistics (all N > ~20,000 cases) to identify isoform- and gene-level associations with six cancers (breast, endometrial, colorectal, lung, ovarian, prostate) and six related cancer subtype classifications (N = 12 total).

Results: Directly modeling isoforms using transcriptome-wide association studies (isoTWAS) significantly improves discovery of genetic associations compared to gene-level approaches, identifying 164% more significant associations (6163 vs. 2336) with isoTWAS-prioritized genes enriched 4-fold for evolutionarily-constrained genes. isoTWAS tags transcriptomic associations at 52% more independent GWAS loci across the six cancers. Isoform expression mediates an estimated 63% greater proportion of cancer risk SNP heritability compared to gene expression. We highlight several isoTWAS associations that demonstrate GWAS colocalization at the isoform level but not at the gene level, including CLPTM1L (lung cancer), LAMC1 (colorectal), and BABAM1 (breast).

Conclusion: These results underscore the importance of modeling isoforms to maximize discovery of genetic risk mechanisms for cancers.

Keywords

Humans, Genome-Wide Association Study, Genetic Predisposition to Disease, Female, Male, Polymorphism, Single Nucleotide, Neoplasms, Protein Isoforms, Lung Neoplasms, Transcriptome, Breast Neoplasms, Prostatic Neoplasms, Gene Expression Profiling, Alternative Splicing, Ovarian Neoplasms, Colorectal Neoplasms, Endometrial Neoplasms, Cancer genomics, Cancer genetics, Gene regulation

Published Open-Access

yes

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