Nicotine triggers initiation and progression of K-Ras driven pancreatic ductal adenocarcinoma via acinar cell de-differentiation
PC Hermann, P Sancho, P Michl, T Gress, R De Pascual, L Gandia, M Canamero, C Guerra, M Barbacid, A Aicher, P Martinelli, FX Real, B Sainz Jr, C Heeschen · Zeitschrift für Gastroenterologie · 2014 · Heft 08
Bibliografische Angaben
Zusammenfassung
Background: Smoking has been identified as a leading risk factor for pancreatic ductal adenocarcinoma. Nicotine is a key active ingredient of tobacco smoke and replacement products, and while nicotine does not have intrinsic carcinogenic properties, we hypothesized that nicotine perpetuates oncogenic transformation of the pancreas by alternative mechanisms. Methods & Results: Using Elastase-K-RasG12V and PDX1-K-RasG12DTrp53R172 H mouse models of pancreatic cancer, we demonstrate that nicotine promotes PanIN and PDAC development. These effects were independent of groß inflammation as nicotine treatment did not in…
