Membrane Estrogen and HER-2 Receptors in Human Breast Cancer

Abstract

Patients with breast cancers that express estrogen receptor (ER) commonly receive antiestrogen therapy. The efficacy of this treatment depends on close regulation of breast growth by estrogen. However, as breast cancers progress, they often become resistant to estrogens, and most patients no longer respond to antiestrogen therapy. New antiestrogen treatment options are needed, and alternative therapies may derive from findings showing that some ER molecules occur in plasma membranes of breast cancer cells and interact with transmembrane HER-2 growth factor receptors. Expression of HER-2 receptors occurs in many breast cancers, and the protein kinase activity of HER-2 may modulate ligand-independent activation of ER. If active cross-communication between ER and HER-2 receptor occurs and leads to promotion of cancer growth, this axis may offer a new target for therapeutic intervention. We are assessing the nature of membrane ER and its rote in promoting the growth of breast cancers. From this work, we hope to develop new treatment options to prevent cancer progression in models of human breast cancer. Since overexpression of HER-2 receptor in breast cancer is associated with failure of antiestrogen therapy in the clinic, understanding the biologic basis of associations between membrane ER and HER-2 receptors may help to improve patient management and enhance survival.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2001
Accession Number
ADA396895

Entities

People

  • Richard J. Pietras

Organizations

  • University of California, Los Angeles

Tags

DTIC Thesaurus Topics

  • Breast Cancer
  • Carrier Proteins
  • Cell Line
  • Cell Membrane
  • Cell Physiological Processes
  • Cells
  • Cellular Structures
  • Chemistry
  • Endocrine Glands
  • Estrogens
  • Growth Factors
  • Hormones
  • Neurons
  • Oncology
  • Proteins
  • Subcellular Fractions
  • Tumor Cell Line

Fields of Study

  • Medicine

Readers

  • Breast cancer cell signaling and growth regulation.