Documents in the NTIS Technical Reports collection are the results of federally funded research. They are directly submitted to or collected by NTIS from Federal agencies for permanent accessibility to industry, academia and the public.  Before purchasing from NTIS, you may want to check for free access from (1) the issuing organization's website; (2) the U.S. Government Printing Office's Federal Digital System website http://www.gpo.gov/fdsys; (3) the federal government Internet portal USA.gov; or (4) a web search conducted using a commercial search engine such as http://www.google.com.
Accession Number ADA566644
Title Mechanism of Prostate Cancer Prevention by Down-Regulation of the GH/IGF Axis.
Publication Date Jul 2012
Media Count 13p
Personal Author S. M. Swanson
Abstract The purpose of this project was to test the hypothesis that growth hormone (GH) stimulates specific pathways, some of which are independent of IGF- I, for promoting proliferation and inhibiting death in prostate cancer cells. Our first aim is to determine which of the multiple signaling pathways stimulated by GH receptor are required to promote prostate cancer. Our strategy was to cross mice that develop prostate cancers due to a large T antigen (TAg) transgene with mice that lack discrete segments of the intracellular portion of the GH receptor. We have not yet completed this experiment due to insufficient breeder fecundity. To assess the relative contribution of IGF-I and GH to prostate carcinogenesis, we grafted prostate tissue harboring the TAg transgene. The grafts were either Ghr+/+ or Ghr-/- and therefore were able to respond to IGF-I but not detect GH. Our results suggest that IGF-I is the major driver of carcinogenesis. We also planned to propagate human prostate cancer cells in vitro and expose them to a human growth hormone antagonist. In vitro, however, the cells were neither stimulated by recombinant human GH nor inhibited by GH antagonist.
Keywords Antigens
Breeder reactors
Cells(Biology)
Growth substances
Oncogenesis
Prostate cancer
Sense organs
Surgical transplantation


 
Source Agency Non Paid ADAS
NTIS Subject Category 57A - Anatomy
57S - Physiology
57E - Clinical Medicine
Corporate Author Chicago Univ., IL.
Document Type Technical report
Title Note Annual rept. 1 Jul 2011-30 Jun 2012.
NTIS Issue Number 1307
Contract Number W81XWH-09-1-0399

Science and Technology Highlights

See a sampling of the latest scientific, technical and engineering information from NTIS in the NTIS Technical Reports Newsletter

Acrobat Reader Mobile    Acrobat Reader