Suppression of Prostate Tumor Progression by Bin 1

Abstract

This project seeks to determine the consequences of deleting Bin1, a gene encoding a Myc-interacting adapter protein with features of a tumor suppressor, for normal development or neoplastic transformation of the mouse prostate. In Year 2 of the project, we identified and resolved by use of an alternate strategy a pitfall in the use of the initial knockout' mouse strains obtained. Specifically, the Cre-mediated strategy for Bin1 knockout in mouse prostate was found to be inoperational in the strains used. As an alternate approach, we have generated mosaic mice that are heterozygous or nullizygous for Bin1 through the animal, including in the prostate. Mice that are highly mosaic for Bin1 knockout in the prostate are being monitored currently for effects on prostate development and tumorigenesis. Additionally, we crossed an activated Myc allele into the mosaic lineage to generate mice that have sustained Myc lesions and frequent Bin1 knockout in the prostate. These mice are being monitored currently for effects of Bin1 loss on conversion of Myc-induced prostatic intraepithelial neoplasia (PIN) to frank carcinoma.

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Document Details

Document Type
Technical Report
Publication Date
Feb 01, 2005
Accession Number
ADA435398

Entities

People

  • George C. Prendergast

Tags

DTIC Thesaurus Topics

  • Breast Cancer
  • Cancer
  • Carcinoma
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Epithelial Cells
  • Genetics
  • Health Services
  • Lymphocytes
  • Neoplasms
  • Prostate Cancer
  • Proteins
  • Stem Cells

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics