Targeting the epigenome for the treatment and prevention of lung cancer

Semin Oncol. 2005 Oct;32(5):488-502. doi: 10.1053/j.seminoncol.2005.07.007.


Alterations in chromatin structure resulting from aberrant DNA methylation and perturbations of the histone code profoundly influence gene expression during pulmonary carcinogenesis. Recent studies indicate that DNA demethylating agents and histone deacetylase (HDAC) inhibitors synergistically induce gene expression and apoptosis in cultured lung cancer cells, and prevent lung cancer development in animals following exposure to tobacco carcinogens. Preliminary clinical trials have established proof of principle regarding the use of DNA demethylating agents and HDAC inhibitors for enhancing immunogenicity and apoptosis of lung cancer cells, and have revealed the complexities concerning the mechanisms by which chromatin remodeling agents mediate antitumor effects in vivo. These data support additional investigations pertaining to the epigenetics of lung cancer, and the evaluation of chromatin remodeling agents for the treatment and prevention of this disease.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Apoptosis
  • Cell Line, Tumor
  • Chromatin / metabolism
  • Clinical Trials as Topic
  • DNA Methylation
  • Enzyme Inhibitors / pharmacology
  • Epigenesis, Genetic*
  • Flow Cytometry
  • Gene Expression Regulation, Neoplastic*
  • Histone Deacetylase Inhibitors
  • Histones / metabolism
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / prevention & control*
  • Time Factors


  • Antineoplastic Agents
  • Chromatin
  • Enzyme Inhibitors
  • Histone Deacetylase Inhibitors
  • Histones