DNA methylation in thoracic neoplasms

Cancer Lett. 2011 Feb 1;301(1):7-16. doi: 10.1016/j.canlet.2010.10.017. Epub 2010 Nov 18.

Abstract

Thoracic neoplasms, which include lung cancers, esophageal carcinoma, and thymic epithelial tumors, are the leading causes of tumor-related death and a major health concern worldwide. The development of neoplasms is a multistep process involving both genetic and epigenetic alterations. A growing body of research provides evidence that aberrant DNA methylation, including DNA hypermethylation in promoter regions, global DNA hypomethylation and the overexpression of DNA methyltransferases, plays an important role in tumorigenesis. In this review, we summarize published observations of methylation pattern disruptions in thoracic tumors, and discuss how these abnormalities contribute to the development of cancers. We review recent findings showing that suppressing the activity of the DNA methylating enzymes DNMTs can have potent anti-cancer effects, and discuss the possibility of developing novel therapies for thoracic tumors based on DNMT inhibition.

Publication types

  • Review

MeSH terms

  • DNA (Cytosine-5-)-Methyltransferase 1
  • DNA (Cytosine-5-)-Methyltransferases / physiology
  • DNA Methylation*
  • Esophageal Neoplasms / genetics
  • Humans
  • Lung Neoplasms / genetics
  • Neoplasms, Glandular and Epithelial / genetics
  • Thoracic Neoplasms / genetics*
  • Thymus Neoplasms / genetics

Substances

  • DNA (Cytosine-5-)-Methyltransferase 1
  • DNA (Cytosine-5-)-Methyltransferases

Supplementary concepts

  • Thymic epithelial tumor