title: Prostate tumor development and androgen receptor function alterations in a new mouse model with ERG overexpression and PTEN inactivation.
abstract: Gene fusions involving ETS transcription factors (predominantly ERG and ETV1) and PTEN deletions are prevalent in the prostate cancer genome. This report describes a novel mouse model that overexpresses ERG and lacks PTEN with the majority of mice developing prostate tumors by 6 mo. Biological mechanisms suggest increased/altered binding of the male hormone receptor in the genome. This model will be useful in pre-clinical evaluation of new drugs targeting these common prostate cancer genomic alterations.
authors.affiliation: Genitourinary Malignancies Branch; Center for Cancer Research; National Cancer Institute; Bethesda, MD USA.
authors.forename: Anjali
authors.initials: A
authors.lastname: Srivastava
authors.affiliation: Genitourinary Malignancies Branch; Center for Cancer Research; National Cancer Institute; Bethesda, MD USA.
authors.forename: Douglas K
authors.initials: DK
authors.lastname: Price
authors.affiliation: Genitourinary Malignancies Branch; Center for Cancer Research; National Cancer Institute; Bethesda, MD USA.
authors.forename: William D
authors.initials: WD
authors.lastname: Figg
mesh_terms: D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000473:pathology*; D005796:Genes / Q000235:genetics*; D006801:Humans; D008297:Male; D051059:PTEN Phosphohydrolase / Q000172:deficiency*; D011471:Prostatic Neoplasms / Q000473:pathology*; D050783:Proto-Oncogene Proteins c-ets / Q000378:metabolism*; D011944:Receptors, Androgen / Q000235:genetics* / Q000378:metabolism*
chemical_list: D050783:Proto-Oncogene Proteins c-ets; D011944:Receptors, Androgen; D051059:PTEN Phosphohydrolase
keywords: ERG; PTEN; androgen receptor; mouse model; prostate