Faster DNA Damage in IBD Underlies Higher Risk of Colorectal Cancer, Study Suggests

Faster DNA Damage in IBD Underlies Higher Risk of Colorectal Cancer, Study Suggests
A high rate of DNA damage in colon cells underlies the increased risk for colorectal cancer associated with inflammatory bowel disease (IBD), according to a recent study. The study, "Somatic Evolution in Non-neoplastic IBD-Affected Colon," was published in the journal Cell. Somatic mutations — those acquired after birth, rather than being inherited — can contribute to cancer development, but their patterns, burden, and functional consequences in other diseases have been less frequently investigated. In the study, researchers from the Wellcome Sanger Institute and Cambridge University Hospitals analyzed tissue from the colonic epithelium (cell layer that forms the lining of the colon) to investigate how somatic mutations arise and spread. The colonic epithelium is organized into millions of folds called crypts, each containing a small population of continually-dividing and renewing stem cells. The research team hypothesized that the cycles of inflammation, ulceration, and regeneration of the colon that occur over the course of IBD might increase DNA damage in these cells, leading to higher mutation rates. Understanding this process could provide insights into the relationship between IBD and colorectal cancer. The team sequenced the genomes of 446 individual crypts from 46 IBD patients and compared their results to those of 412 crypts from 41 healthy people. The researchers discovered that IBD-associated crypt cells contained over twice the number of somatic mutations as healthy tissue and that the number of mutations rose with the duration of IBD. “We found that normal mutational processes that are operative in us all are accelerated in the IBD affected gut, leading to a more than two-fold increase in the rate at which some gut cells acqui
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