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. Our current data suggest that at least two co-activators of ER, i.e., SPA and AIE1, 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 previous results together with our current 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 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, 2000
Accession Number
ADB266306

Entities

People

  • Leigh C. Murphy

Organizations

  • University of Manitoba

Tags

DTIC Thesaurus Topics

  • Breast Cancer
  • Carcinoma
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Estrogens
  • Gene Expression
  • Genetics
  • Governments
  • Health Services
  • Hormones
  • Information Science
  • Medical Personnel
  • Neoplasms
  • Oncology
  • Prostate Cancer

Fields of Study

  • Medicine

Readers

  • Breast cancer cell signaling and growth regulation.