TGF-β1 promotes acinar to ductal metaplasia of human pancreatic acinar cells
Author:
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/srep30904.pdf
Reference39 articles.
1. Kopp, J. L. et al. Identification of Sox9-Dependent Acinar-to-Ductal Reprogramming as the Principal Mechanism for Initiation of Pancreatic Ductal Adenocarcinoma. Cancer Cell 22, 737–750 (2012).
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3. Zhu, L., Shi, G., Schmidt, C. M., Hruban, R. H. & Konieczny, S. F. Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia. Am. J. Pathol. 171, 263–273 (2007).
4. Bailey, J. M., DelGiorno, K. E. & Crawford, H. C. The secret origins and surprising fates of pancreas tumors. Carcinogenesis 35, 1436–1440 (2014).
5. Shi, G. et al. Maintenance of acinar cell organization is critical to preventing Kras-induced acinar-ductal metaplasia. Oncogene 32, 1950–1958 (2013).
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