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Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal...
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Serrated pathway in colorectal carcinogenesis.

Letícia Yamane1, Cristovam Scapulatempo-Neto1, Rui Manuel Reis1

  • 1Letícia Yamane, Rui Manuel Reis, Denise Peixoto Guimarães, Molecular Oncology Research Center, Barretos Cancer Hospital, Barretos, 14780-000 São Paulo, Brazil.

World Journal of Gastroenterology
|March 15, 2014
PubMed
Summary

Serrated polyps are precursors to a distinct colorectal cancer (CRC) subtype. Understanding their unique molecular pathways and clinical features is crucial for developing effective CRC prevention and treatment strategies.

Keywords:
Colorectal carcinogenesisCpG island methylator phenotypeMicrosatellite instabilityMutationSerrated pathway

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Area of Science:

  • Gastroenterology and Oncology
  • Molecular Pathology

Background:

  • Serrated adenocarcinoma is a distinct colorectal cancer (CRC) subtype, originating from serrated polyps instead of traditional adenomas.
  • Serrated polyps encompass hyperplastic polyps (HPs), sessile serrated adenomas (SSAs), and traditional serrated adenomas (TSAs), with HPs being the most common.

Purpose of the Study:

  • To review current knowledge on serrated polyps, including their clinical-pathological features.
  • To update findings on the molecular pathways involved in serrated colorectal cancer development.

Main Methods:

  • Literature review of serrated polyps and serrated adenocarcinoma.
  • Analysis of genetic and molecular alterations in the serrated pathway.

Main Results:

  • Serrated polyps represent approximately 10% of all colorectal cancers.
  • Key genetic factors include KRAS and BRAF mutations, alongside microsatellite instability and CpG island methylator phenotype.
  • Distinct histogenesis influences prevention, prognosis, and therapeutic strategies.

Conclusions:

  • Understanding the biology and malignant potential of serrated polyps is essential for CRC prevention.
  • Implementing targeted surveillance approaches for serrated lesions can aid in preventing colorectal cancer development.