Co-Operation Between FADD and Bin1 in Prostate Cancer Apoptosis

Abstract

This project studied a novel apoptosis pathway that is induced by the death domain of the adaptor protein FADD (FADD-DD). This pathway is important because it represents a very early defect in the development of prostate cancer and links a novel cell death pathway to the immortalization and transformation of epithelial cells. The current project is based on the finding that the tumor suppressor Bin1 can co-operate with FADD-DD to kill a prostate tumor cell line (LNCaP) that is normally resistant to FADD-DD and the grant was intended to understand the role of Bin1 in this signaling pathway. During the funding period, we achieved the goals outlined in the original grant. Moreover we were able to extend these studies in other directions and achieve goals that were not in the original grant. This work was reported in the literature and ongoing studies that are nearing completion will generate further scientific publications. In addition, based on findings supported by the award, we were able to develop a new research proposal that received RO1 funding from NCI to continue this work.

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Apr 01, 2006
Accession Number
ADA458416

Entities

People

  • Andrew M. Thorburn

Organizations

  • University of Colorado Health

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Diseases And Disorders
  • Enzyme Inhibitors
  • Epithelial Cells
  • Mammary Glands
  • Neoplasms
  • Programmed Cell Death
  • Prostate Cancer
  • Proteins
  • Three Dimensional
  • Tissues
  • Tumor Cell Line

Readers

  • Clinical Trial Research.
  • Molecular Biology and Genetics
  • Oncology (Cancer Research).