Accession Number:

ADA508242

Title:

Mechanisms of Abnormal Growth Regulation in Prostatic Adenocarcinoma Using Abi1/Hssh3bp1 Conditional Knockout Mouse Model

Descriptive Note:

Annual rept. 19 May 2008-18 May 2009

Corporate Author:

NEW YORK BLOOD CENTER NY

Personal Author(s):

Report Date:

2009-06-01

Pagination or Media Count:

70.0

Abstract:

Prostate cancer is the most common type of cancer found in American men. The American Cancer Society estimates that there will be about 190,000 new cases and 27,000 deaths of prostate cancer in the United States in 2009. Genetic alterations of tumor suppressor genes are one of the most common causes of prostate cancer tumorigenesis. Our group identified Abi1Hssh3bp1 as candidate prostate tumor suppressor gene. To understand the role of Abi1Hssh3bp1 in prostate tumorigenesis we developed the conditional Abi1Hssh3bp1 KO mouse. In the first funding period we expanded our mouse colony and set up specific breeding schemes for proposed prostate tumorigenesis mouse models i.e. for prostate-specific disruption of Abi1Hssh3bp1 or simultaneous disruption of Abi1Hssh3bp1 and PTEN genes. Cre recombinase-mediated disruption of the gene was confirmed in dissected prostates of animals with Abi1Hssh3bp1 flflPbCreTg- genotype. In addition we isolated Abi1Hssh3bp1 flfl MEF cells and cloned cells lacking Abi1Hssh3bp1 to be used for in vitro characterization of Abi1Hssh3bp1-dependent cell growth regulation pathways. Toward that goal we also screened genomewide SH2 domain library with phosphotyrosine peptides derived from Abi1Hssh3bp1 and identified several candidate Abi1Hssh3bp1-binding SH2 domain-containing proteins. These protein-Abi1Hssh3bp1 interactions will be further characterized using cells and animal tissue lacking Abi1Hssh3bp1.

Subject Categories:

  • Medicine and Medical Research

Distribution Statement:

APPROVED FOR PUBLIC RELEASE