NSBCC

Project 4 Publications

Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer Cancer Cell 4 209-221

Download this file

Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer.

Wang S, Gao J, Lei Q, Rozengurt N, Pritchard C, Jiao J, Thomas GV, Li G, Roy-Burman P, Nelson PS, Liu X, Wu H.

Howard Hughes Medical Institute, University of California Los Angeles School of Medicine, 90095, Los Angeles, CA, USA

The murine Pten prostate cancer model described in this study recapitulates the disease progression seen in humans: initiation of prostate cancer with prostatic intraepithelial neoplasia (PIN), followed by progression to invasive adenocarcinoma, and subsequent metastasis with defined kinetics. Furthermore, while Pten null prostate cancers regress after androgen ablation, they are capable of proliferating in the absence of androgen. Global assessment of molecular changes caused by homozygous Pten deletion identified key genes known to be relevant to human prostate cancer, including those "signature" genes associated with human cancer metastasis. This murine prostate cancer model provides a unique tool for both exploring the molecular mechanism underlying prostate cancer and for development of new targeted therapies.

Related Categories: Project 4 PublicationsNSBCC Publications

Myc-driven murine prostate cancer...Cancer Cell 2003:(4) 223-238 (Sawyers)

Download this file
Increased Myc gene copy number is observed in human prostate cancer. To define Myc's functional role, we generated transgenic mice expressing human c-Myc in the mouse prostate. All mice developed murine prostatic intraepithelial neoplasia followed by invasive adenocarcinoma. Microarray-based expression profiling identified a Myc prostate cancer expression signature, which included the putative human tumor suppressor NXK3.1. Human prostate tumor databases revealed modules of human genes that varied in concert with the Myc prostate cancer signature. This module includes the Pim-1 kinase, a gene known to cooperate with Myc in tumorigenesis, and defines a subset of human, "Myc-like" human cancers.
Related Categories: Project 4 PublicationsNSBCC Publications
Grab the RSS newsfeed for this category:
XML feed
HomeAbout NSBCCPeopleProjectsContact UsLogin
© 2005, NSBCC: NanoSystems Biology Cancer Center
Caltech Chemistry 127-72 1200 East California Blvd.
Pasadena, CA 91125