A Novel Apoptosis Pathway that is Defective in Early Breast Cancer

Abstract

This project studies a novel apoptosis pathway that is induced by the death domain of the adaptor protein FADD (FADD-DD) . This pathway can induce apoptosis only in normal epithelial cells from the breast (or prostate) and its inactivation may represent an early defect that arises in breast cancer. SV4O T antigen can selectively block this apoptosis pathway. The overall goal of this project is to investigate and further understand why breast cancer cells are resistant to this apoptosis pathway. As outlined in the previous progress report, we achieved all the goals for aim 1 and made new observations that allow alternate approaches to address the project. Importantly we showed that mouse breast epithelial cells display the same apoptosis response to FADD-DD. The reviewer of our previous progress report suggested that we study this response in the absence of Sv4OT antigen since this would be more applicable to actual breast cancer. We therefore continued with our studies as outlined in the statement of work and expanded our studies in mouse cells that allow us to avoid the use of Sv4O T antigen. Our data show that inactivation of the p53, Rb, INK4a/ARF pathways do not explain resistance to this apoptosis.

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Document Details

Document Type
Technical Report
Publication Date
Apr 01, 2004
Accession Number
ADA425681

Entities

People

  • Andrew M. Thorburn
  • D. Phil

Organizations

  • Wake Forest University

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Biomedical Research
  • Breast Cancer
  • Cell Physiological Processes
  • Cells
  • Epithelial Cells
  • Genes
  • Molecules
  • Neoplasms
  • North Carolina
  • Proteins
  • Resistance

Readers

  • Cellular and Molecular Pathways of Apoptosis.
  • Oncology (Cancer Research).
  • Prostate Cancer Biology.