Document Detail


Loss of PTEN is associated with progression to androgen independence.
MedLine Citation:
PMID:  16496415     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Progression to a lethal androgen-independent (AI) stage of advanced prostate cancer is a critical clinical obstacle limiting patient survival. PTEN inactivation is frequently observed in advanced prostate cancer and correlates with a poor prognosis. However, the functional significance of PTEN inactivation in AI progression has not been demonstrated. METHODS: PTEN expression was examined in benign, hormone naïve and AI human prostate cancer specimens, and in recurrent AI Shionogi tumors. The effect of antisense oligonucleotide (ASO)-mediated PTEN downregulation in AI progression of the Shionogi tumor model was determined. RESULTS: Significantly reduced PTEN expression was observed in AI versus benign and hormone naïve prostate tumors. Seven of 14 AI Shionogi tumors exhibited marked downregulation or complete loss of PTEN. ASO-mediated PTEN inhibition reduced androgen-withdrawal induced regression of Shionogi tumors and accelerated AI progression. CONCLUSIONS: These data suggest that PTEN inactivation may play a role in progression to androgen independence.
Authors:
Jerod Bertram; James W Peacock; Ladan Fazli; Alice L-F Mui; Stephen W Chung; Michael E Cox; Brett Monia; Martin E Gleave; Christopher J Ong
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Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  The Prostate     Volume:  66     ISSN:  0270-4137     ISO Abbreviation:  Prostate     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-05-15     Completed Date:  2006-07-05     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8101368     Medline TA:  Prostate     Country:  United States    
Other Details:
Languages:  eng     Pagination:  895-902     Citation Subset:  IM    
Copyright Information:
Copyright 2006 Wiley-Liss, Inc.
Affiliation:
The Prostate Centre, Vancouver General Hospital, Vancouver, British Columbia, Canada.
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MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / physiology
Androgens / analysis,  physiology*
Animals
Blotting, Northern
Blotting, Western
Disease Progression
Down-Regulation
Gene Expression Regulation, Neoplastic / drug effects
Genes, Suppressor / physiology
Humans
Male
Mice
Mice, Inbred Strains
Neoplasm Staging
Oligonucleotides, Antisense / pharmacology
PTEN Phosphohydrolase / genetics*,  physiology*
Prognosis
Prostatic Neoplasms / chemistry,  genetics*,  physiopathology*
Signal Transduction / physiology
Chemical
Reg. No./Substance:
0/Androgens; 0/Oligonucleotides, Antisense; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 3.1.3.48/PTEN protein, human; EC 3.1.3.67/PTEN Phosphohydrolase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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