Tumor Suppressor Mechanism in Breast Cancer: Studies in Genetically Engineered Mice

Abstract

The p53 and pRb tumor suppressor pathways are frequently altered in human breast cancer. Although animal models have begun to explore mechanisms for these proteins, the roles can be different depending on the cancer type. Our previous studies in a mouse brain epithelial tumor model have demonstrated the importance of pRb in tumor initiation and of p53 in tumor progression, and have established p53-dependent apoptosis as a means of tumor suppression. In this model, brain cells are induced to proliferate aberrantly by tissue-specific expression of T121, a small T antigen oncoprotein that inactivates pRb. This causes slow growing, but highly apoptotic tumors. Further inactivation of p53 causes a dramatic decline in cell death and rapid acceleration of tumor growth. We propose similar studies to examine the pRb and p53 roles in breast cancer. The full T antigen oncoprotein (inactivates both pRb and p53) has been shown to induce mammary tumors in transgenic mice. Here, the T - oncoprotein will be tissue-specifically expressed in mammary epithelium by mammary-specific promoters to test the role of pRb.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2002
Accession Number
ADA410072

Entities

People

  • Terry A. Van Dyke

Organizations

  • University of North Carolina at Chapel Hill

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Biomedical Research
  • Breast Cancer
  • Cancer
  • Cell Physiological Processes
  • Cells
  • Connective Tissue
  • Epithelial Cells
  • Epithelium
  • Genetically Modified Organisms
  • Genetics
  • Mammary Glands
  • Neoplasms
  • North Carolina
  • Suppressors
  • Tissues

Fields of Study

  • Biology
  • Medicine

Readers

  • Molecular Biology and Genetics

Technology Areas

  • Biotechnology
  • Biotechnology - Cancer Biotech