The Estrogen Receptor and Its Variants as Risk Factors in Breast Cancer

Abstract

The overall goal of this research is to understand how the estrogen receptor (ER) signal transduction pathway is altered during breast tumorigenesis and if altered ER signal transduction increases the risk of developing breast cancer. Our previous data suggest that altered expression of ER alpha, ER beta and their variants occurs during breast tumorigenesis. Current data suggest that at least two co-activators of ER, i.e., SRA and AIB1, as well as activated MAP kinase, that can activate ER in a ligand independent fashion, are significantly increased during breast tumorigenesis. In contrast, a repressor of ER activity (REA) is not significantly altered during breast tumorigenesis. Our results suggest that multiple factors involved in estrogen receptor mediated signal transduction, are altered during human breast tumorigenesis and may have a role in the development of breast. Some of these factors e.g., active MAP kinase, are also altered between pre-invasive and invasive breast cancer. These data are consistent with the hypothesis that alterations of ER signal transduction occurring during the early stages of pre-neoplastic progression may effect the risk of developing breast cancer.

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Document Details

Document Type
Technical Report
Publication Date
Nov 01, 2001
Accession Number
ADA405667

Entities

People

  • Leigh Murph

Organizations

  • University of Manitoba

Tags

DTIC Thesaurus Topics

  • Breast Cancer
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Drug Therapy
  • Gene Expression
  • Genetics
  • Health Services
  • Medical Personnel
  • Neoplasms
  • Oncology

Readers

  • Breast cancer cell signaling and growth regulation.