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Transcriptome-wide Mendelian randomization exploring dynamic CD4+ T cell gene expression in colorectal cancer development

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F25%3A00639029" target="_blank" >RIV/68378041:_____/25:00639029 - isvavai.cz</a>

  • Result on the web

    <a href="https://academic.oup.com/jleukbio/advance-article/doi/10.1093/jleuko/qiaf131/8257067?searchresult=1" target="_blank" >https://academic.oup.com/jleukbio/advance-article/doi/10.1093/jleuko/qiaf131/8257067?searchresult=1</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1093/jleuko/qiaf131" target="_blank" >10.1093/jleuko/qiaf131</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Transcriptome-wide Mendelian randomization exploring dynamic CD4+ T cell gene expression in colorectal cancer development

  • Original language description

    Recent research suggests higher circulating lymphocyte counts may protect against colorectal cancer (CRC). However, the role of specific lymphocyte subtypes and activation states remain unclear. CD4+ T cells – a highly dynamic lymphocyte subtype – undergo gene expression changes upon activation that are critical to their effector function. Previous studies using bulk tissue have limited our understanding of their role in CRC risk to static associations. We applied Mendelian randomization (MR) and genetic colocalisation to evaluate causal relationships of gene expression on CRC risk across multiple CD4+ T cell subtypes and activation states. Genetic proxies were obtained from single-cell transcriptomic data, allowing us to investigate the causal effect of expression of 1,805 genes across CD4+ T cell activation states on CRC risk (78,473 cases, 107,143 controls). Analyses were stratified by CRC anatomical subsites and sex, with sensitivity analyses assessing whether the observed effect estimates were likely to be CD4+ T cell-specific. We identified six genes – FADS2, FHL3, HLA-DRB1, HLA-DRB5, RPL28, and TMEM258 – with strong evidence for a causal role in CRC development (FDR-P<0.05, colocalisation H4>0.8). Causal estimates varied by CD4+ T cell subtype, activation state, CRC subsite and sex. However, many of genetic proxies used to instrument gene expression in CD4+ T cells also act as eQTLs in other tissues, highlighting the challenges of using genetic proxies to instrument tissue-specific expression changes. We demonstrate the importance of capturing the dynamic nature of CD4+ T cells in understanding CRC risk, and prioritize genes for further investigation in cancer prevention.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>ost</sub> - Miscellaneous article in a specialist periodical

  • CEP classification

  • OECD FORD branch

    30204 - Oncology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2025

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Journal of Leukocyte Biology

  • ISSN

    0741-5400

  • e-ISSN

    1938-3673

  • Volume of the periodical

    117

  • Issue of the periodical within the volume

    10

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    37

  • Pages from-to

    giaf131

  • UT code for WoS article

  • EID of the result in the Scopus database