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A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
06:01

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Published on: July 6, 2017

A comprehensive strategy to combat colon cancer targeting the adenomatous polyposis coli tumor suppressor gene

Eugene W Gerner1, Natalia A Ignatenko, Peter Lance

  • 1The University of Arizona, Arizona Cancer Center, Tucson, AZ 85724, USA. egerner@azcc.arizona.edu

Annals of the New York Academy of Sciences
|December 31, 2005
PubMed

Insights

Mutations in the adenomatous polyposis coli (APC) gene are common in colorectal cancer. APC influences genes like c-Myc and ornithine decarboxylase (ODC), offering potential targets for cancer prevention and therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Somatic mutations/deletions in the adenomatous polyposis coli (APC) tumor suppressor gene are prevalent in colorectal polyps and cancers.
  • APC plays a crucial role in normal intestinal development and cellular processes.
  • Loss of APC function is linked to intestinal neoplasia in both mice and humans.

Purpose of the Study:

  • To investigate the role of APC and its downstream genes in colorectal cancer development.
  • To explore the potential of APC-dependent genes as biomarkers for colorectal cancer risk.
  • To evaluate APC-dependent genes as targets for colorectal cancer chemoprevention and therapy.

Main Methods:

  • Analysis of APC gene mutations in colorectal tumors.
  • Examination of APC's influence on the expression of c-Myc and ornithine decarboxylase (ODC).
  • Review of existing research on single nucleotide polymorphisms (SNPs) in the ODC promoter and their association with cancer risk.

Main Results:

  • Loss of APC function leads to alterations in c-Myc-regulated genes, including ODC, the key enzyme in polyamine synthesis.
  • A specific ODC promoter SNP affecting c-Myc-dependent expression is associated with increased risk of colorectal and other cancers.
  • Pharmaceuticals targeting the c-Myc promoter are being developed for colorectal cancer therapy, and difluoromethylornithine (DFMO), an ODC inhibitor, is in clinical trials for chemoprevention.

Conclusions:

  • APC and its regulated genes, c-Myc and ODC, are critical in colorectal tumorigenesis.
  • These genes represent potential genetic markers for assessing colorectal cancer risk.
  • APC-dependent genes offer promising targets for the development of novel chemopreventive and therapeutic strategies for colorectal cancer.

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