Estrogen Effects on Breast Tumor Growth in Estrogen Receptor-Minus Mice

Abstract

Although nearly half of human breast cancers at diagnosis are estrogen-responsive and respond to antiestrogen therapy at least for a time, more than half are estrogen receptor negative (ER-) and are predicted to be estrogen-nonresponsive tumors. However, some tumors which are ER- appear to respond to antiestrogen therapy in patients, which is beneficial because antihormonal therapy is less toxic than the alternative chemotherapy. The SCID mouse model has been recently used to study the hormonal dependence of growth of human breast cancer cells as tumors. Recent work has identified a potential model system where ER- breast cancer cells are estrogen- independent in cell culture, and yet intriguingly show estrogen-stimulated growth as tumors in SCID mice. This model system will extend understanding of the host contribution to tumor growth by isolating the host portion of estrogen-stimulated breast tumor growth. The potential to control tumor growth by modulating the host animal mechanism would be of particular value in the treatment of estrogen-nonresponsive tumors which recur alter "breakthrough" of tamoxifen therapy, as well as tumors that are ER- and assumed to be estrogen-nonresponsive at diagnosis. Understanding how estrogens can lead to the increased growth of estrogens-nonresponsive breast tumors may lead to new mechanisms to better control the growth of estrogens-independent breast cancer.

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Document Details

Document Type
Technical Report
Publication Date
Sep 01, 1998
Accession Number
ADA382532

Entities

People

  • Dennis B. Lubahn

Organizations

  • University of Missouri

Tags

DTIC Thesaurus Topics

  • Anti-Bacterial Agents
  • Blood
  • Breast Cancer
  • Carcinoma
  • Cell Line
  • Cells
  • Chemistry
  • Culture Techniques
  • Gene Expression
  • Genetics
  • Hormones
  • Immune System
  • Medical Personnel
  • Mrna
  • Neoplasms
  • Proteins
  • Tumor Cell Line

Readers

  • Molecular Biology and Genetics
  • Oncology
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