Programmed Cell Death in Breast Cancer

Abstract

A model system for investigating the fundamental mechanisms of programmed cell death, apoptosis, in breast cancer cells has been developed. This model is based on the induction of apoptosis by the calcium pump inhibitor, thapsigargin. Our results indicate that thapsigargin induced apoptosis in breast cancer cells is mediate through caspase activation and is inhibited by Bcl-2. Also, we have found that lymphoma cells are much for susceptible to thapsigargin induced apoptosis than breast cancer cells. Our results indicate that this difference in susceptibility to apoptosis is due to the ability of breast cancer cells to mount a protective stress response that is absent in lymphoma cells. Understanding the mechanism of apoptosis through use of this model system should provide a basis for developing new therapies for breast cancer, based on abrogating endogenous cellular stress responses that reduce susceptibility to apoptosis induction.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 1997
Accession Number
ADA340671

Entities

People

  • Clark W. Distelhorst

Organizations

  • Case Western Reserve University

Tags

DTIC Thesaurus Topics

  • Amino Acids
  • Animal Structures
  • Apoptosis
  • Biomedical Research
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemical Synthesis
  • Chemistry
  • Culture Techniques
  • Endoplasmic Reticulum
  • Health Services
  • Inhibitors
  • Neoplasms
  • Programmed Cell Death
  • Proteins
  • Tumor Cell Line

Fields of Study

  • Biology

Readers

  • Cellular and Molecular Pathways of Apoptosis.
  • Molecular Biology and Genetics