Regulation of Retinoid Responsiveness in Mammary Carcinoma Cells.

Abstract

The data presented in this annual report support our hypothesis for a mechanism of retinoid-induced growth arrest of human breast cancer cells. Specifically, we believe that retinoids inhibit human breast cancer cell proliferation by inducing a state of functional mitogen deprivation. Kinetic and quantitative changes in cell cycle progression and gene expression following retinoic acid treatment of the estrogen dependent, T-47D breast cancer cell line, are consistent with retinoic acid inducing a block in the treated cells' ability to respond to external mitogenic signals.

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Document Details

Document Type
Technical Report
Publication Date
Sep 01, 1996
Accession Number
ADA327148

Entities

People

  • David A. Talmage

Organizations

  • Columbia University

Tags

DTIC Thesaurus Topics

  • Acids
  • Breast Cancer
  • Carcinoma
  • Carrier Proteins
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemical Synthesis
  • Chemistry
  • Deprivation
  • Gene Expression
  • Growth Factors
  • Hormones
  • Molecules
  • Neoplasms
  • New York
  • Proteins

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.
  • Theoretical Analysis.