Cancer epigenetics comes of age

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Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
07:50

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer

Published on: September 18, 2020

P A Jones1, P W Laird

  • 1Department of Biochemistry and Molecular Biology, University of Southern California School of Medicine, The Norris Comprehensive Cancer Center, Los Angeles 90033, USA. jones_p@froggy.hsc.usc.edu

Nature Genetics
|February 13, 1999
PubMed

Insights

DNA methylation, a key epigenetic mechanism, silences tumour-suppressor genes in cancer. This process, involving hypermethylated promoters, contributes to malignant transformation and genetic damage, expanding cancer gene inactivation models.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • DNA methylation is increasingly recognized as a significant mechanism in cancer development.
  • Hypermethylation of tumour-suppressor gene promoters leads to gene silencing.
  • Epigenetic alterations can promote genetic instability and cancer progression.

Purpose of the Study:

  • To review the current understanding of DNA methylation's role in cancer.
  • To highlight how DNA methylation contributes to tumour-suppressor gene inactivation.
  • To propose an expansion of existing cancer models to include epigenetic mechanisms.

Main Methods:

  • Literature review of mechanistic studies on DNA methylation in cancer.
  • Analysis of the link between DNA methylation, gene silencing, and genetic damage.
  • Synthesis of current knowledge to inform cancer aetiology models.

Main Results:

  • Numerous tumour-suppressor genes are inactivated via promoter hypermethylation.
  • DNA methylation can increase mutagenicity and silence critical DNA repair genes (e.g., MLH1).
  • Epigenetic events are integral to malignant transformation alongside genetic alterations.

Conclusions:

  • DNA methylation is a crucial alternative pathway for tumour-suppressor inactivation in cancer.
  • Epigenetic mechanisms, including DNA methylation, play a direct role in facilitating genetic damage.
  • Knudson's two-hit hypothesis should be updated to incorporate epigenetic gene inactivation in cancer models.

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