Programmed Cell Death in Breast Cancer.

Abstract

A model system for investigating the fundamental mechanism of programmed cell death, apoptosis, in breast cancer cells has been developed. This model is based on induction of apoptosis by the selective endoplasmic reticulum calcium pump inhibitor, thapsigargin. Thapsigargin induced apoptosis is inhibited by Bcl-2 and is mediated by activation of cysteine proteases belonging to the interleukin 1-Beta converting enzyme family. The decision of a cell to undergo apoptosis following thasigargin treatment is regulated, in part, by the capacity of the cell to induce transcription of the grp78 stress response gene. Understanding the mechanism of apoptosis through use of this model system should provide a basis for developing new therapies for breast cancer.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 1996
Accession Number
ADB221966

Entities

People

  • Clark W. Distelhorst

Organizations

  • Case Western Reserve University

Tags

DTIC Thesaurus Topics

  • Amino Acids
  • Animal Structures
  • Apoptosis
  • Biomedical Research
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Endoplasmic Reticulum
  • Inhibitors
  • Materials
  • Neoplasms
  • Programmed Cell Death
  • Prostate Cancer
  • Tumor Cell Line

Fields of Study

  • Biology

Readers

  • Molecular and Cellular Biochemistry
  • Oncology (Cancer Research).