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Differential gene expression in inflamed mucosa of progressed UC patients compared to inflamed mucosa of non-progressed UC patients

ABSTRACT: A small percentage of ulcerative colitis patients may experience disease progression into colitis-associated colorectal cancer (CA-CRC). In the clinic, it is challenging to identify these patients. Consequently, all UC patients are followed closely by e.g. annual colonoscopy from eight years of the UC diagnosis. Although, the progression may still be difficult to discover as the neoplastic mucosa may appear with a flat structure. The need for biomarkers that early in the UC disease course can predict the predisposition to progress into CA-CRC is therefore highly wanted in the clinic. The objective of this gene expression analysis was to identify a set of genes with differential expression in inflamed mucosa of progressed UC patients compared to inflamed mucosa of non-progressed UC patients. The gene expression was examined using Agilent SurePrint G3 human gene expression 60K microarray.

ORGANISM(S): Homo sapiens

PROVIDER: GSE151911 | GEO | 2026/06/15

REPOSITORIES: GEO

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Project description:Introduction: Many gene expression studies of colitis-associated colorectal cancer (CA-CRC) in patients with ulcerative colitis (UC) have focused on identification of molecular drivers of progression of UC to CA- CRC. However, they have primarily studied cancerous mucosal biopsies, an approach which primarily may identify the characteristics of the established cancer mucosa and not the early molecular events driving the progression. Long-standing mucosal inflammation is suspected to be one of the main drivers of CA-CRC. Still, not all patients with UC progress and develop cancer. We hypothesise that patients with UC, who have progressed to neoplasia (progressors), have a different molecular profile of inflammation than non-progressors. Methods: We performed transcriptome profiling on 143 mucosal biopsies from non-neoplastic colonic segments of 14 UC progressors and 30 UC non-progressors. In addition, we performed profiling of lymphocyte infiltration to the mucosa of biopsies taken adjacent to biopsies used for transcriptomic analysis. Results: We found a characteristic gene expression profile for inflamed mucosa of UC progressors, which primarily is associated with progression of UC to dysplasia or cancer as opposed to long duration of disease. The gene expression profile suggests that the inflamed tissue of UC progressors is negatively enriched for biological processes such as adaptive immune responses and complement system activity and positively enriched for biological processes related to detoxification. Moreover, we found that the microenvironment in the inflamed mucosa of progressors differs from non-progressors by having fewer infiltrating B cells and less lymphoid aggregates. Conclusions: We found that inflammation of UC patients, who have progressed to dysplasia or cancer, has a different gene expression profile than that of UC non-progressors. Importantly, this profile was primarily associated with progression of disease as opposed to duration of disease. The inflamed mucosa of UC progressors may have lower levels of lymphoid organ-initiating and immune cell- attracting signals and fewer immune cells infiltrating the mucosa. Consequently, progressors may lack the ability to mount sufficient adaptive immune responses necessary to counteract driving forces of malignant transformation in UC.

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Differential gene expression in inflamed mucosa of progressed UC patients compared to inflamed mucosa of non-progressed UC patients

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