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Title:

Selective requirement of PI3K/PDK1 signaling for Kras oncogene-driven pancreatic cell plasticity and cancer.

Document type:
Journal Article; Research Support, Non-U.S. Gov't
Author(s):
Eser, S; Reiff, N; Messer, M; Seidler, B; Gottschalk, K; Dobler, M; Hieber, M; Arbeiter, A; Klein, S; Kong, B; Michalski, CW; Schlitter, AM; Esposito, I; Kind, AJ; Rad, L; Schnieke, AE; Baccarini, M; Alessi, DR; Rad, R; Schmid, RM; Schneider, G; Saur, D
Abstract:
Oncogenic Kras activates a plethora of signaling pathways, but our understanding of critical Ras effectors is still very limited. We show that cell-autonomous phosphoinositide 3-kinase (PI3K) and 3-phosphoinositide-dependent protein kinase 1 (PDK1), but not Craf, are key effectors of oncogenic Kras in the pancreas, mediating cell plasticity, acinar-to-ductal metaplasia (ADM), and pancreatic ductal adenocarcinoma (PDAC) formation. This contrasts with Kras-driven non-small cell lung cancer, where...     »
Journal title abbreviation:
Cancer Cell
Year:
2013
Journal volume:
23
Journal issue:
3
Pages contribution:
406-20
Language:
eng
Fulltext / DOI:
doi:10.1016/j.ccr.2013.01.023
Pubmed ID:
http://view.ncbi.nlm.nih.gov/pubmed/23453624
Print-ISSN:
1535-6108
TUM Institution:
Chirurgische Klinik und Poliklinik; II. Medizinische Klinik und Poliklinik (Gastroenterologie); Institut für Allgemeine Pathologie und Pathologische Anatomie
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