The Roles of Histone Deacetylase and DNA Methylation in Estrogen Receptor alpha Expression in Breast Cancer

Abstract

The proposal tests the hypothesis that histone deacetylase activity contributes to the transcriptional repression of the methylated estrogen receptor alpha (ER) gene. It further postulates that inhibition of histone deacetylase (HDAC) and DNA methylation may act together to reactivate the ER gene. Studies to date show that the HDAC inhibitor trichostatin A, can reactivate ER expression in ER-negative breast cancer cell line. Combined treatment with HDAC inhibitors and demethylating agents can synergistically reactivate expression of ER-negative breast cancer cell lines.

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Document Details

Document Type
Technical Report
Publication Date
Jun 01, 2003
Accession Number
ADA421800

Entities

People

  • Yi Huang

Organizations

  • Johns Hopkins Hospital

Tags

DTIC Thesaurus Topics

  • Breast Cancer
  • Carcinogens
  • Carcinoma
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemical Synthesis
  • Chemistry
  • Chromosomes
  • Colon Cancer
  • Enzyme Inhibitors
  • Genetics
  • Neoplasms
  • Oncology
  • Ovarian Cancer
  • Tumor Cell Line

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.
  • Molecular Biology and Genetics