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    Early-onset colorectal cancer (CRC) shows accelerated DNA methylation aging. Epigenetic changes, not microbes, may drive sporadic cases in young adults, suggesting a role for accelerated aging in EOCRC development.

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    Area of Science:

    • Oncology
    • Genetics
    • Epigenetics

    Background:

    • Colorectal cancer (CRC) incidence is rising in young adults (<50 years).
    • The causes of most early-onset CRC (EOCRC) are unknown, despite germline mutations in ~20% of cases.
    • Non-genetic factors like environment and lifestyle are suspected contributors to sporadic EOCRC.

    Purpose of the Study:

    • To investigate differences in the epigenome, microbiome, and immunome between EOCRC and average-onset CRC (AOCRC).
    • To identify potential etiological factors for sporadic EOCRC.

    Main Methods:

    • Compared DNA methylation patterns in EOCRC and AOCRC patients using The Cancer Genome Atlas (TCGA) data.
    • Identified intra-tumoral microbes and deconvolved immune cell abundances across TCGA and two additional datasets.
    • Validated epigenetic findings using gene expression data from TCGA and the Oncology Research Information Exchange Network (ORIEN).

    Main Results:

    • EOCRC patients exhibited DNA methylation age acceleration by 12 years compared to AOCRC patients.
    • Differentially methylated sites were linked to CREB signaling, G protein coupled receptor signaling, phagosome formation, and S100 family signaling.
    • No consistent differences in intra-tumoral microbes were found, but microbial interactions with the immune system differed between EOCRC and AOCRC.

    Conclusions:

    • Epigenetic modulation and accelerated aging are implicated in the development of EOCRC.
    • While microbes did not differ consistently, their immune interactions varied, suggesting a complex interplay.
    • Further research into epigenetic mechanisms is warranted for understanding and potentially treating EOCRC.