p53 suppresses type II endometrial carcinomas in mice and governs endometrial tumour aggressiveness in humans
作者: Peter J. WildKristian IkenbergThomas J. FuchsMarkus RechsteinerStrahil GeorgievNiklaus FankhauserAurelia NoskeMatthias RoessleRosmarie CaduffAthanassios DellasDaniel FinkHolger MochWilhelm KrekIan J. Frew
作者单位: 1Institute of Surgical Pathology, University Hospital Zurich, Zurich, Switzerland
2 Department of Electrical Engineering, California Institute of Technology, Pasadena, CA, USA
3 Institute of Cell Biology, ETH Zurich, Zurich, Switzerland
4 Department of Pathology, University Hospital Basel, University of Basel, Basel, Switzerland
5 Department of Gynaecology, University Hospital Zurich, Zurich, Switzerland
6 Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland
7 Tel: +41 44 635 50 04; Fax: +41 44 635 6814
刊名: EMBO Molecular Medicine, 2012, Vol.4 (8), pp.808-824
来源数据库: Wiley Journal
DOI: 10.1002/emmm.201101063
关键词: clear cellendometrial carcinomamouse modelp53serous
原始语种摘要: Abstract(#br)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...
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