ArticleClinical and experimental gastroenterology2025
Colonic Mucosal Gene Expression Profile in Patients with Neoplastic Progression in Longstanding Ulcerative Colitis.
Article in Clinical and experimental gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- The Role of Nuclear APOBEC Enzymes in Neoplastic Progression of Ulcerative Colitis.Clinical and experimental gastroenterology · 2026Article
- Exploring the Relationship Between Colitis-Associated Cancer and Lipid Metabolism Reprogramming from the Perspective of Inflammation-Cancer Transformation.Journal of inflammation research · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Long-standing mucosal inflammation is suspected to be one of the main drivers of colitis-associated colorectal cancer (CA-CRC), but far from all colitis patients develop cancer. Non-neoplastic mucosa located distant from neoplastic lesions may harbour early molecular events of carcinogenesis. We hypothesise that patients with UC who have progressed to neoplasia (progressors) exhibit a distinct molecular profile of mucosal inflammation from non-progressors. Patients and Methods: We performed transcriptomic profiling of 143 mucosal biopsies from non-neoplastic colonic segments of 14 UC progressors and 30 UC non-progressors using the Agilent SurePrint G3 human gene expression 60K microarray. Subsequently, we carried out gene set ontology analyses. In addition, we assessed lymphocyte infiltration to the mucosa of biopsies taken adjacent to biopsies used for transcriptomic analysis by immunohistochemistry. Results: Adjusting for molecular alterations associated with long disease duration, our findings revealed that UC Progressors' inflamed mucosa has a distinct gene expression profile of 529 significantly deregulated genes, eg Conclusion: The inflamed colonic mucosa from UC patients who have progressed to dysplasia or cancer has a different gene expression profile than that of UC non-progressors, suggesting lower levels of lymphoid organ-initiating and immune cell-attracting signals and fewer infiltrating immune cells to 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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