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• W2004616054 abstract "You have accessJournal of UrologyProstate Cancer: Basic Research1 Apr 2011740 PROSTATE TUMOR GROWTH IN PBARR2-CRE PTEN KNOCKOUT MICE IS DELAYED IN GH/IGF-I DEFICIENT MICE Kiyoshi Takahara, Naokazu Ibuki, Howard Tearle, Haruhito Azuma, Yoji Katsuoka, Martin E.Gleave, Christopher J. Ong, Michael Pollak, and Michael E. Cox Kiyoshi TakaharaKiyoshi Takahara Takatsuki, Osaka, Japan More articles by this author , Naokazu IbukiNaokazu Ibuki Vancouver, Canada More articles by this author , Howard TearleHoward Tearle Vancouver, Canada More articles by this author , Haruhito AzumaHaruhito Azuma Takatsuki, Osaka, Japan More articles by this author , Yoji KatsuokaYoji Katsuoka Takatsuki, Osaka, Japan More articles by this author , Martin E.GleaveMartin E.Gleave Vancouver, Canada More articles by this author , Christopher J. OngChristopher J. Ong Vancouver, Canada More articles by this author , Michael PollakMichael Pollak Montreal, Canada More articles by this author , and Michael E. CoxMichael E. Cox Vancouver, Canada More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2011.02.1709AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Growth hormone/insulin-like growth factor I (GH/IGF-I) axis has been related to risk of prostate cancer (PCa). We have previously reported that androgen-responsive, castration-resistant (CR), and androgen-independent (AI) PCa xenografts develop more slowly in little murine hosts. The little (lit/lit) phenotype is due to a D60G missense mutation in the GH-releasing hormone receptor (GHRHR) resulting in loss of pituitary GHRHR function and suppression of GH and IGF-I expression. PTEN is a tumor suppressor gene that is frequently mutated in a variety of spontaneous cancers, including PCa. The prostate-conditional PTEN-null mouse represents the first animal model in which deletion of a single endogenous gene leads to invasive PCa. METHODS To investigate the role of GH/IGF-I axis on in vivo prostate carcinogenesis and neoplastic progression, we crossed pbARR2-Cre, PTEN(fl/fl) mice (PTEN−/−) with IGF-I deficient lit mice, and produced lit/lit and lit/+ PTEN−/− mice. To complement the in vivo experiments, in vitro growth and growth factor signaling of murine PTEN−/− cells derived from the prostate (MPPK) or lymph node (MLPK) using serum from lit/lit or lit/+ mice was examined. RESULTS Body weight and serum GH, IGF-I levels of lit/lit PTEN−/− mice were significantly reduced as compared with lit/+ PTEN−/− mice. At 15 weeks of age, prostate cancer progression of lit/lit PTEN−/− mice was partially delayed as compared with lit/+ PTEN−/− mice. MPPK and MLPK cells growth in vitro with serum from lit/lit mice showed decreased proliferation as compared with serum from lit/+ mice. Suppressed growth in lit/lit serum could be restored by addition of IGF-I, and to a lesser extent, GH. Addition of GH or IGF-I to lit/lit serum increased only activation of AKT while no change in ERK1/2 activation was detected in MPPK cells. CONCLUSIONS Our in vivo and in vitro results suggest that prostate carcinogenesis may be influenced by germ line variation of genes encoding signaling molecules in the GH/IGF-I axis and support the continued development of clinical trials of novel hormonal treatment strategies that target the GH/IGF-I axis for PCa patients. © 2011 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 185Issue 4SApril 2011Page: e297 Advertisement Copyright & Permissions© 2011 by American Urological Association Education and Research, Inc.MetricsAuthor Information Kiyoshi Takahara Takatsuki, Osaka, Japan More articles by this author Naokazu Ibuki Vancouver, Canada More articles by this author Howard Tearle Vancouver, Canada More articles by this author Haruhito Azuma Takatsuki, Osaka, Japan More articles by this author Yoji Katsuoka Takatsuki, Osaka, Japan More articles by this author Martin E.Gleave Vancouver, Canada More articles by this author Christopher J. Ong Vancouver, Canada More articles by this author Michael Pollak Montreal, Canada More articles by this author Michael E. Cox Vancouver, Canada More articles by this author Expand All Advertisement Advertisement PDF DownloadLoading ..." @default.
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• W2004616054 title "740 PROSTATE TUMOR GROWTH IN PBARR2-CRE PTEN KNOCKOUT MICE IS DELAYED IN GH/IGF-I DEFICIENT MICE" @default.
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