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Epigenetic Alterations in Colitis-Associated Colorectal Cancer

  • bgtaylor1
  • Feb 24
  • 1 min read

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Date:

January 16, 2026

PMID:

Category:

N/A

Authors:

Nisha Ganesh, William M Grady, Andrew M Kaz

Abstract:


Colitis-associated colorectal cancer (CAC) represents a distinct subtype of colorectal malignancy that arises in the setting of chronic inflammatory bowel disease (IBD). Unlike sporadic colorectal cancer, CAC develops through inflammation-driven molecular pathways, in which epigenetic alterations play a pivotal role in tumor initiation and progression. This review highlights the major epigenetic mechanisms implicated in CAC, including DNA methylation, histone modifications, and microRNA (miRNA) dysregulation. Aberrant DNA methylation patterns, such as promoter hypermethylation of tumor suppressor genes and global hypomethylation, contribute to genomic instability and altered gene expression. In parallel, inflammation-induced changes in histone configuration modulate chromatin accessibility and transcriptional activity of key oncogenic and tumor-suppressive pathways. Furthermore, deregulated miRNAs influence multiple aspects of CAC pathogenesis by targeting genes involved in inflammation and tumor progression. Understanding these epigenetic processes provides valuable insights into the development of colorectal malignancy and identifies potential biomarkers for early detection and intervention in colitis-associated colorectal cancer.


Acknowledgements:

The content of this article is solely the responsibility of the authors and does not necessarily represent the official views of the National Cancer Institute, or the National Institute of Health.


The Translational and Basic Science Research in Early Lesions (TBEL) Research Consortia is supported and funded by grants from the National Cancer Institute and the National Institutes of Health under the following award numbers:


Project Number:

Awardee Organization

U54CA274374

Fred Hutchinson Cancer Center

U54CA274375

Houston Methodist Research Institute

U54CA274370

Johns Hopkins University

U54CA274371

UT MD Anderson Cancer Center

U54CA274367

Vanderbilt University Medical Center


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