FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2789802671> ?p ?o ?g. }

• W2789802671 endingPage "14471" @default.
• W2789802671 startingPage "14456" @default.
• W2789802671 abstract "// Longjiang Shao 1, 2 , Jianghua Wang 1, 2 , Omer Faruk Karatas 1, 2 , Shu Feng 1, 2 , Yiqun Zhang 3, 4 , Chad J. Creighton 3, 4 and Michael Ittmann 1, 2 1 Deptartment of Pathology & Immunology, Baylor College of Medicine, Houston, Texas 77030, USA 2 Michael E. DeBakey Department of Veterans Affairs Medical Center, Houston, Texas 77030, USA 3 Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA 4 Dan L. Duncan Cancer Center Division of Biostatistics, Baylor College of Medicine, Houston, Texas 77030, USA Correspondence to: Michael Ittmann, email: mittmann@bcm.edu Keywords: prostate cancer; signal transduction; fibroblast growth factors; PTEN; TMPRSS2/ERG Abbreviations: PCa: prostate cancer; TE: TMPRSS2/ERG; FGF: fibroblast growth factors; KD: knockdown Received: December 05, 2017      Accepted: February 03, 2018      Epub: February 12, 2018     Published: March 06, 2018 ABSTRACT Prostate cancer is the most common visceral malignancy and the second leading cause of cancer deaths in US men. Correlative studies in human prostate cancers reveal a frequent association of the TMPRSS2/ERG (TE) fusion gene with loss of PTEN and studies in mouse models reveal that ERG expression and PTEN loss synergistically promote prostate cancer progression. To determine the mechanism by which ERG overexpression and PTEN loss leads to transformation, we overexpressed the TE fusion gene and knocked down PTEN in an immortalized but non-transformed prostate epithelial cell line. We show that ERG overexpression in combination with PTEN loss can transform these immortalized but non-tumorigenic cells, while either alteration alone was not sufficient to fully transform these cells. Expression microarray analysis revealed extensive changes in gene expression in cells expressing the TE fusion with loss of PTEN. Among these gene expression changes was increased expression of multiple FGF ligands and receptors. We show that activation of fibroblast growth factor receptor signaling plays a key role in transformation induced by TE fusion gene expression in association with PTEN loss. In addition, in vitro and in silico analysis reveals PTEN loss is associated with widespread increases in FGF ligands and receptors in prostate cancer. Inhibitors of FGF receptor signaling are currently entering the clinic and our results suggests that FGF receptor signaling is a therapeutic target in cancers with TE fusion gene expression and PTEN loss." @default.
• W2789802671 created "2018-03-29" @default.
• W2789802671 creator A5007587959 @default.
• W2789802671 creator A5022815457 @default.
• W2789802671 creator A5037121973 @default.
• W2789802671 creator A5049425681 @default.
• W2789802671 creator A5066263660 @default.
• W2789802671 creator A5082311544 @default.
• W2789802671 creator A5086954044 @default.
• W2789802671 date "2018-02-12" @default.
• W2789802671 modified "2023-09-26" @default.
• W2789802671 title "Fibroblast growth factor receptor signaling plays a key role in transformation induced by the TMPRSS2/ERG fusion gene and decreased PTEN" @default.
• W2789802671 cites W1520162011 @default.
• W2789802671 cites W1527661581 @default.
• W2789802671 cites W1540577611 @default.
• W2789802671 cites W1858086881 @default.
• W2789802671 cites W1917376867 @default.
• W2789802671 cites W1984285831 @default.
• W2789802671 cites W1986799557 @default.
• W2789802671 cites W1992079095 @default.
• W2789802671 cites W1998566859 @default.
• W2789802671 cites W2001779392 @default.
• W2789802671 cites W2003793248 @default.
• W2789802671 cites W2003866931 @default.
• W2789802671 cites W2004477123 @default.
• W2789802671 cites W2006619657 @default.
• W2789802671 cites W2015437876 @default.
• W2789802671 cites W2026081337 @default.
• W2789802671 cites W2029988036 @default.
• W2789802671 cites W2039015433 @default.
• W2789802671 cites W2049205984 @default.
• W2789802671 cites W2052428706 @default.
• W2789802671 cites W2068879625 @default.
• W2789802671 cites W2072620890 @default.
• W2789802671 cites W2079298594 @default.
• W2789802671 cites W2082462837 @default.
• W2789802671 cites W2087045997 @default.
• W2789802671 cites W2089567904 @default.
• W2789802671 cites W2094252220 @default.
• W2789802671 cites W2102174623 @default.
• W2789802671 cites W2106054588 @default.
• W2789802671 cites W2106570439 @default.
• W2789802671 cites W2107633226 @default.
• W2789802671 cites W2110017050 @default.
• W2789802671 cites W2119765426 @default.
• W2789802671 cites W2121158863 @default.
• W2789802671 cites W2121214880 @default.
• W2789802671 cites W2124194872 @default.
• W2789802671 cites W2130410032 @default.
• W2789802671 cites W2131316990 @default.
• W2789802671 cites W2138645479 @default.
• W2789802671 cites W2139900107 @default.
• W2789802671 cites W2141077390 @default.
• W2789802671 cites W2145355816 @default.
• W2789802671 cites W2149441684 @default.
• W2789802671 cites W2152881862 @default.
• W2789802671 cites W2159686118 @default.
• W2789802671 cites W2165757793 @default.
• W2789802671 cites W2168346858 @default.
• W2789802671 cites W2168471784 @default.
• W2789802671 cites W2170552969 @default.
• W2789802671 cites W2325246333 @default.
• W2789802671 cites W2563337881 @default.
• W2789802671 cites W2612076693 @default.
• W2789802671 doi "https://doi.org/10.18632/oncotarget.24470" @default.
• W2789802671 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5865682" @default.
• W2789802671 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29581856" @default.
• W2789802671 hasPublicationYear "2018" @default.
• W2789802671 type Work @default.
• W2789802671 sameAs 2789802671 @default.
• W2789802671 citedByCount "5" @default.
• W2789802671 countsByYear W27898026712019 @default.
• W2789802671 countsByYear W27898026712020 @default.
• W2789802671 countsByYear W27898026712021 @default.
• W2789802671 crossrefType "journal-article" @default.
• W2789802671 hasAuthorship W2789802671A5007587959 @default.
• W2789802671 hasAuthorship W2789802671A5022815457 @default.
• W2789802671 hasAuthorship W2789802671A5037121973 @default.
• W2789802671 hasAuthorship W2789802671A5049425681 @default.
• W2789802671 hasAuthorship W2789802671A5066263660 @default.
• W2789802671 hasAuthorship W2789802671A5082311544 @default.
• W2789802671 hasAuthorship W2789802671A5086954044 @default.
• W2789802671 hasBestOaLocation W27898026711 @default.
• W2789802671 hasConcept C103796816 @default.
• W2789802671 hasConcept C104317684 @default.
• W2789802671 hasConcept C111829193 @default.
• W2789802671 hasConcept C118487528 @default.
• W2789802671 hasConcept C121608353 @default.
• W2789802671 hasConcept C126322002 @default.
• W2789802671 hasConcept C143998085 @default.
• W2789802671 hasConcept C2777609662 @default.
• W2789802671 hasConcept C2778042024 @default.
• W2789802671 hasConcept C2779134260 @default.
• W2789802671 hasConcept C2780192828 @default.
• W2789802671 hasConcept C2780827179 @default.
• W2789802671 hasConcept C3008058167 @default.
• W2789802671 hasConcept C502942594 @default.
• W2789802671 hasConcept C524204448 @default.

• next