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Purpose of Review <p>Colorectal cancer (CRC) is a complex, multifactorial disease that progresses from benign polyps to invasive malignancy. Understanding the genetic and molecular mechanisms driving this transition is crucial for advancing early detection, risk stratification, and therapeutic strategies. This review provides a comprehensive analysis of shared and distinct genetic signatures, their interplay with the tumor microenvironment (TME), and their clinical implications for CRC management.</p> Recent Findings <p>Genetic alterations associated with CRC progression are intricately linked to key molecular pathways, including WNT, MAPK, and PI3K/AKT, which regulate tumor initiation, growth, and metastasis. Dysregulation of long non-coding RNAs such as PVT1 and MALAT1 contributes to CRC predisposition and prognosis. Additionally, miR-187-3p plays a crucial role in metastasis, with its target gene SPRY1 offering potential therapeutic intervention. The tumor microenvironment (TME) significantly influences CRC progression, with gut microbiota dysbiosis emerging as a critical factor. Specific bacterial strains, such as pks + Escherichia coli and Fusobacterium nucleatum, induce DNA damage, chronic inflammation, and immune evasion, further promoting carcinogenesis. Microbiota-derived metabolites, including short-chain fatty acids and polyamines, have been identified as potential therapeutic targets, highlighting the role of dietary modifications in CRC prevention.</p> Summary <p>This review provides an in-depth exploration of the molecular pathways governing the transition from colorectal polyps to CRC. Existing literature has limitations, either due to the absence of a recent comprehensive review or reliance on outdated perspectives. By addressing these gaps, this study enhances the understanding of genetic, epigenetic, and environmental factors influencing CRC progression. The findings underscore the need for precision medicine approaches, integrating genomic profiling and microbiome-targeted therapies, to improve early detection, prognostication, and patient outcomes.</p> Graphical Abstract <p></p>

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Genetic Signatures Upon Transition from Colorectal Polyps to colon Cancer

  • 期刊论文

  • 发表日期：

    2025年4月12日

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  • Mehran Radak,
  • Farahnoosh Khodabakhsh Ravand,
  • Nakisa Ghamari,
  • Hossein Fallahi

摘要

Purpose of Review

Colorectal cancer (CRC) is a complex, multifactorial disease that progresses from benign polyps to invasive malignancy. Understanding the genetic and molecular mechanisms driving this transition is crucial for advancing early detection, risk stratification, and therapeutic strategies. This review provides a comprehensive analysis of shared and distinct genetic signatures, their interplay with the tumor microenvironment (TME), and their clinical implications for CRC management.

Recent Findings

Genetic alterations associated with CRC progression are intricately linked to key molecular pathways, including WNT, MAPK, and PI3K/AKT, which regulate tumor initiation, growth, and metastasis. Dysregulation of long non-coding RNAs such as PVT1 and MALAT1 contributes to CRC predisposition and prognosis. Additionally, miR-187-3p plays a crucial role in metastasis, with its target gene SPRY1 offering potential therapeutic intervention. The tumor microenvironment (TME) significantly influences CRC progression, with gut microbiota dysbiosis emerging as a critical factor. Specific bacterial strains, such as pks + Escherichia coli and Fusobacterium nucleatum, induce DNA damage, chronic inflammation, and immune evasion, further promoting carcinogenesis. Microbiota-derived metabolites, including short-chain fatty acids and polyamines, have been identified as potential therapeutic targets, highlighting the role of dietary modifications in CRC prevention.

Summary

This review provides an in-depth exploration of the molecular pathways governing the transition from colorectal polyps to CRC. Existing literature has limitations, either due to the absence of a recent comprehensive review or reliance on outdated perspectives. By addressing these gaps, this study enhances the understanding of genetic, epigenetic, and environmental factors influencing CRC progression. The findings underscore the need for precision medicine approaches, integrating genomic profiling and microbiome-targeted therapies, to improve early detection, prognostication, and patient outcomes.

Graphical Abstract