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dc.contributor.author
Wild, Peter J.
dc.contributor.author
Ikenberg, Kristian
dc.contributor.author
Fuchs, Thomas J.
dc.contributor.author
Rechsteiner, Markus
dc.contributor.author
Georgiev, Strahil
dc.contributor.author
Fankhauser, Niklaus
dc.contributor.author
Noske, Aurelia
dc.contributor.author
Rössle, Matthias
dc.contributor.author
Caduff, Rosmarie
dc.contributor.author
Dellas, Athanassios
dc.contributor.author
Fink, Daniel
dc.contributor.author
Moch, Holger
dc.contributor.author
Krek, Wilhelm
dc.contributor.author
Frew, Ian J.
dc.date.accessioned
2019-08-16T11:56:50Z
dc.date.available
2017-06-10T07:51:06Z
dc.date.available
2019-08-16T11:56:50Z
dc.date.issued
2012-08-01
dc.identifier.issn
1757-4676
dc.identifier.issn
1757-4684
dc.identifier.other
10.1002/emmm.201101063
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/54290
dc.identifier.doi
10.3929/ethz-b-000054290
dc.description.abstract
Type II endometrial carcinomas are a highly aggressive group of tumour subtypes that are frequently associated with inactivation of the TP53 tumour suppressor gene. We show that mice with endometrium‐specific deletion of Trp53 initially exhibited histological changes that are identical to known precursor lesions of type II endometrial carcinomas in humans and later developed carcinomas representing all type II subtypes. The mTORC1 signalling pathway was frequently activated in these precursor lesions and tumours, suggesting a genetic cooperation between this pathway and Trp53 deficiency in tumour initiation. Consistent with this idea, analyses of 521 human endometrial carcinomas identified frequent mTORC1 pathway activation in type I as well as type II endometrial carcinoma subtypes. mTORC1 pathway activation and p53 expression or mutation status each independently predicted poor patient survival. We suggest that molecular alterations in p53 and the mTORC1 pathway play different roles in the initiation of the different endometrial cancer subtypes, but that combined p53 inactivation and mTORC1 pathway activation are unifying pathogenic features among histologically diverse subtypes of late stage aggressive endometrial tumours.
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-nc/3.0/
dc.subject
Clear cell
en_US
dc.subject
Endometrial carcinoma
en_US
dc.subject
Mouse model
en_US
dc.subject
p53
en_US
dc.subject
Serous
en_US
dc.title
p53 suppresses type II endometrial carcinomas in mice and governs endometrial tumour aggressiveness in humans
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution-NonCommercial 3.0 Unported
dc.date.published
2012-06-08
ethz.journal.title
EMBO Molecular Medicine
ethz.journal.volume
4
en_US
ethz.journal.issue
8
en_US
ethz.journal.abbreviated
EMBO Mol Med
ethz.pages.start
808
en_US
ethz.pages.end
824
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 / Krek, Wilhelm
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 / Krek, Wilhelm
ethz.date.deposited
2017-06-10T07:51:31Z
ethz.source
ECIT
ethz.identifier.importid
imp59364fa633acd55226
ethz.ecitpid
pub:87726
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-15T07:09:49Z
ethz.rosetta.lastUpdated
2019-08-16T11:57:01Z
ethz.rosetta.versionExported
true
ethz.COinS
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