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Status: Bibliographieeintrag

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Verfasst von:Maass, Thorsten [VerfasserIn]   i
 Thieringer, Florian R. [VerfasserIn]   i
 Mann, Amrit [VerfasserIn]   i
 Longerich, Thomas [VerfasserIn]   i
 Schirmacher, Peter [VerfasserIn]   i
 Strand, Dennis [VerfasserIn]   i
 Hansen, Torsten [VerfasserIn]   i
 Galle, Peter R. [VerfasserIn]   i
 Teufel, Andreas [VerfasserIn]   i
 Kanzler, Stephan [VerfasserIn]   i
Titel:Liver specific overexpression of platelet-derived growth factor-B accelerates liver cancer development in chemically induced liver carcinogenesis
Verf.angabe:Thorsten Maass, Florian R. Thieringer, Amrit Mann, Thomas Longerich, Peter Schirmacher, Dennis Strand, Torsten Hansen, Peter R. Galle, Andreas Teufel and Stephan Kanzler
Jahr:2011
Umfang:10 S.
Fussnoten:Online puliziert: 20 May 2010 ; Gesehen am 22.11.2022
Titel Quelle:Enthalten in: International journal of cancer
Ort Quelle:Bognor Regis : Wiley-Liss, 1966
Jahr Quelle:2011
Band/Heft Quelle:128(2011), 6, Seite 1259-1268
ISSN Quelle:1097-0215
Abstract:A genetic basis of hepatocellular carcinoma (HCC) has been well-established and major signaling pathways, such as p53, Wnt-signaling, transforming growth factor-β (TGF-β) and Ras pathways, have been identified to be essential to HCC development. Lately, the family of platelet-derived growth factors (PDGFs) has shifted to the center of interest. We have reported on spontaneously developing liver fibrosis in PDGF-B transgenic mice. Since HCC rarely occurs in healthy liver, but dramatically increases at the cirrhosis stage of which liver fibrosis is a preliminary stage, we investigated liver cancer development in chemically induced liver carcinogenesis in these mice. HCC induction was performed by treatment of the mice with diethylnitrosamine and phenobarbital. At an age of 6 months, the tumor development of these animals was analyzed. Not only the development of dysplastic lesions in PDGF-B transgenic mice was significantly increased but also their malignant transformation to HCC. Furthermore, we were able to establish a key role of PDGF-B signaling at diverse stages of liver cancer development. Here, we show that development of liver fibrosis is likely through upregulation of TGF-β receptors by PDGF-B. Additionally, overexpression of PDGF-B also leads to an increased expression of β-catenin as well as vascular endothelial growth factor and platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31), all factors with established roles in carcinogenesis. We were able to extend the understanding of key genetic regulators in HCC development by PDGF-B and decode essential downstream signals.
DOI:doi:10.1002/ijc.25469
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1002/ijc.25469
 Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1002/ijc.25469
 DOI: https://doi.org/10.1002/ijc.25469
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:DEN
 HCC
 PDGF-B
 TGF-β
 β-catenin
K10plus-PPN:1823195172
Verknüpfungen:→ Zeitschrift

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