Suppression of Prostate Tumor Progression by Bin 1

Abstract

This project investigated the role of Bin 1, a gene encoding a Myc-interacting adapter protein with features of a tumor suppressor on the normal development or neoplastic transformation of the mouse prostate. In Aim 1 we determined the effect of deleting Bin 1 on normal prostate development and tumorigenesis (tumor suppressor model). In Aim 2 we determined the effect of Bin 1 deletion on neoplastic progression of lesions initiated by a prostate-specific c-Myc gene (negative modifier model). In Year 1 we showed that deletion of the conditional `floxed' allele of Bin 1 phenocopied deletion of the wild-type allele as anticipated. However, to overcome difficulties that arose in Year 2 with generating prostate-specific deletions we created mosaic animals for the study. Although studies are as yet incomplete, results collected to date in Year 3 suggest that Bin 1 loss does not increase prostate cancer incidence nor does it drive progression of Myc-initiated cancers. Ongoing experiments test whether (I.) Bin 1 loss limits castration-induced apoptosis in normal prostate cells and/or (II.) Bin 1 loss phenocopies Myc activation during progression of Ras-driven cancers based on findings about the effects of Bin 1 on Myc stability emerging from other projects in Year 3.

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Document Details

Document Type
Technical Report
Publication Date
Feb 01, 2006
Accession Number
ADA458252

Entities

People

  • George C. Prendergast

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Biomedical Research
  • Cancer
  • Castration
  • Cell Physiological Processes
  • Cells
  • Demographic Cohorts
  • Experimental Design
  • Genes
  • Losses
  • Medical Personnel
  • Neoplasms
  • Prostate
  • Prostate Cancer
  • Standards
  • Tissues

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics