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Titel:

A subset of metastatic pancreatic ductal adenocarcinomas depends quantitatively on oncogenic Kras/Mek/Erk-induced hyperactive mTOR signalling.

Dokumenttyp:
Journal Article; 4
Autor(en):
Kong, Bo; Wu, Weiwei; Cheng, Tao; Schlitter, Anna Melissa; Qian, Chengjia; Bruns, Philipp; Jian, Ziying; Jäger, Carsten; Regel, Ivonne; Raulefs, Susanne; Behler, Nora; Irmler, Martin; Beckers, Johannes; Friess, Helmut; Erkan, Mert; Siveke, Jens T; Tannapfel, Andrea; Hahn, Stephan A; Theis, Fabian J; Esposito, Irene; Kleeff, Jörg; Michalski, Christoph W
Abstract:
Oncogenic Kras-activated robust Mek/Erk signals phosphorylate to the tuberous sclerosis complex (Tsc) and deactivates mammalian target of rapamycin (mTOR) suppression in pancreatic ductal adenocarcinoma (PDAC); however, Mek and mTOR inhibitors alone have demonstrated minimal clinical antitumor activity.We generated transgenic mouse models in which mTOR was hyperactivated either through the Kras/Mek/Erk cascade, by loss of Pten or through Tsc1 haploinsufficiency. Primary cancer cells were isolat...     »
Zeitschriftentitel:
Gut
Jahr:
2016
Band / Volume:
65
Heft / Issue:
4
Seitenangaben Beitrag:
647-57
Sprache:
eng
Volltext / DOI:
doi:10.1136/gutjnl-2014-307616
PubMed:
http://view.ncbi.nlm.nih.gov/pubmed/25601637
Print-ISSN:
0017-5749
TUM Einrichtung:
Chirurgische Klinik und Poliklinik; II. Medizinische Klinik und Poliklinik (Gastroenterologie); Institut für Allgemeine Pathologie und Pathologische Anatomie
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