par Prévot, Pierre-Paul 
;Simion, Alexandru;Grimont, Adrien;Colletti, Marta;Khalaileh, Abed;Van Den Steen, Géraldine ;Sempoux, Christine;Xu, Xiaobo;Roelants, Véronique;Hald, Jacob;Bertrand, Luc;Heimberg, Harry;Konieczny, Stephen F;Dor, Yuval;Lemaigre, Frédéric P;Jacquemin, Patrick
Référence Gut, 61, 12, page (1723-1732)
Publication Publié, 2012-12
;Simion, Alexandru;Grimont, Adrien;Colletti, Marta;Khalaileh, Abed;Van Den Steen, Géraldine ;Sempoux, Christine;Xu, Xiaobo;Roelants, Véronique;Hald, Jacob;Bertrand, Luc;Heimberg, Harry;Konieczny, Stephen F;Dor, Yuval;Lemaigre, Frédéric P;Jacquemin, PatrickRéférence Gut, 61, 12, page (1723-1732)
Publication Publié, 2012-12
Article révisé par les pairs
| Résumé : | Growing evidence suggests that a phenotypic switch converting pancreatic acinar cells to duct-like cells can lead to pancreatic intraepithelial neoplasia and eventually to invasive pancreatic ductal adenocarcinoma. Histologically, the onset of this switch is characterised by the co-expression of acinar and ductal markers in acini, a lesion called acinar-to-ductal metaplasia (ADM). The transcriptional regulators required to initiate ADM are unknown, but need to be identified to characterise the regulatory networks that drive ADM. In this study, the role of the ductal transcription factors hepatocyte nuclear factor 6 (HNF6, also known as Onecut1) and SRY-related HMG box factor 9 (Sox9) in ADM was investigated. |
