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dc.contributor.author
Albers, Joachim
dc.contributor.author
Rajski, Michal
dc.contributor.author
Schönenberger, Désirée
dc.contributor.author
Harlander, Sabine
dc.contributor.author
Schraml, Peter
dc.contributor.author
von Teichman, Adriana
dc.contributor.author
Georgiev, Strahil
dc.contributor.author
Wild, Peter J.
dc.contributor.author
Moch, Holger
dc.contributor.author
Krek, Wilhelm
dc.contributor.author
Frew, Ian J.
dc.date.accessioned
2019-08-20T13:45:30Z
dc.date.available
2017-06-10T18:11:40Z
dc.date.available
2019-08-20T13:45:30Z
dc.date.issued
2013-06-01
dc.identifier.issn
1757-4676
dc.identifier.issn
1757-4684
dc.identifier.other
10.1002/emmm.201202231
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/68288
dc.identifier.doi
10.3929/ethz-b-000068288
dc.description.abstract
The combinations of genetic alterations that cooperate with von Hippel–Lindau (VHL) mutation to cause clear cell renal cell carcinoma (ccRCC) remain poorly understood. We show that the TP53 tumour suppressor gene is mutated in approximately 9% of human ccRCCs. Combined deletion of Vhl and Trp53 in primary mouse embryo fibroblasts causes proliferative dysregulation and high rates of aneuploidy. Deletion of these genes in the epithelium of the kidney induces the formation of simple cysts, atypical cysts and neoplasms, and deletion in the epithelia of the genital urinary tract leads to dysplasia and tumour formation. Kidney cysts display a reduced frequency of primary cilia and atypical cysts and neoplasms exhibit a pro‐proliferative signature including activation of mTORC1 and high expression of Myc, mimicking several cellular and molecular alterations seen in human ccRCC and its precursor lesions. As the majority of ccRCC is associated with functional inactivation of VHL, our findings suggest that for a subset of ccRCC, loss of p53 function represents a critical event in tumour development.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Wiley
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/3.0/
dc.subject
ccRCC
en_US
dc.subject
Cyst
en_US
dc.subject
p53
en_US
dc.subject
VHL
en_US
dc.title
Combined mutation of Vhl and Trp53 causes renal cysts and tumours in mice
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 3.0 Unported
dc.date.published
2013-04-22
ethz.journal.title
EMBO Molecular Medicine
ethz.journal.volume
5
en_US
ethz.journal.issue
6
en_US
ethz.journal.abbreviated
EMBO Mol Med
ethz.pages.start
949
en_US
ethz.pages.end
964
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.nebis
005874008
ethz.publication.place
Weinheim
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02539 - Institut für Molecular Health Sciences / Institute of Molecular Health Sciences::03630 - Krek, Wilhelm (ehemalig) / Krek, Wilhelm (former)
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::02539 - Institut für Molecular Health Sciences / Institute of Molecular Health Sciences::03630 - Krek, Wilhelm (ehemalig) / Krek, Wilhelm (former)
ethz.date.deposited
2017-06-10T18:11:43Z
ethz.source
ECIT
ethz.identifier.importid
imp593650b51385e64500
ethz.ecitpid
pub:108492
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-18T14:38:52Z
ethz.rosetta.lastUpdated
2019-08-20T13:45:42Z
ethz.rosetta.exportRequired
true
ethz.rosetta.versionExported
true
ethz.COinS
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