# Epigenetic Alterations in Colitis-Associated Colorectal Cancer

## TL;DR

This paper reviews how epigenetic changes contribute to the development of colorectal cancer linked to chronic inflammation in inflammatory bowel disease.

## Contribution

The paper provides a comprehensive overview of epigenetic mechanisms in colitis-associated colorectal cancer, highlighting their role in tumor initiation and progression.

## Key findings

- Epigenetic alterations like DNA methylation and histone modifications are key in colitis-associated colorectal cancer.
- Deregulated miRNAs influence inflammation and tumor progression in CAC.
- Epigenetic changes contribute to genomic instability and altered gene expression in CAC.

## 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.