Literature DB >> 19896097

Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer.

Craig D Logsdon1, Baoan Ji.   

Abstract

The relationship between chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) is unclear. CP is a risk factor for PDAC, CP is found within the vicinity of PDAC, and both share many similar genetic alterations. However, it has been long thought that PDAC arises only from duct cells. However, we have recently found that excessive activity within the Ras signaling pathway can lead to acinar cell death or metaplasia and is associated with the development of fibrosis resembling CP and the development of PDAC from acinar cells through the full complement of preneoplastic (pancreatic intraepithelial neoplasia) lesions. Therefore, it is time to reevaluate the relationship between CP and PDAC. We proposed a new model in which Ras activity is the direct link between these 2 diseases. Here we will briefly review the shared properties between CP and PDAC and describe the new model.

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Year:  2009        PMID: 19896097      PMCID: PMC3050544          DOI: 10.1016/j.cgh.2009.07.040

Source DB:  PubMed          Journal:  Clin Gastroenterol Hepatol        ISSN: 1542-3565            Impact factor:   11.382


  43 in total

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Journal:  Hepatogastroenterology       Date:  1999 Jan-Feb

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Authors:  Therese Deramaudt; Anil K Rustgi
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Authors:  K Takaori; R H Hruban; A Maitra; N Tanigawa
Journal:  Adv Med Sci       Date:  2006       Impact factor: 3.287

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Authors:  Heiko Witt; Minoti V Apte; Volker Keim; Jeremy S Wilson
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9.  The Nestin progenitor lineage is the compartment of origin for pancreatic intraepithelial neoplasia.

Authors:  Catherine Carrière; Elliott S Seeley; Tobias Goetze; Daniel S Longnecker; Murray Korc
Journal:  Proc Natl Acad Sci U S A       Date:  2007-03-05       Impact factor: 11.205

10.  Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice.

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  25 in total

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Review 2.  Animal models of gastrointestinal and liver diseases. Animal models of acute and chronic pancreatitis.

Authors:  Xianbao Zhan; Fan Wang; Yan Bi; Baoan Ji
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Review 3.  Acinar cell plasticity and development of pancreatic ductal adenocarcinoma.

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Journal:  Nat Rev Gastroenterol Hepatol       Date:  2017-03-08       Impact factor: 46.802

4.  Pancreatitis-diabetes-pancreatic cancer: summary of an NIDDK-NCI workshop.

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6.  Transcriptional Maintenance of Pancreatic Acinar Identity, Differentiation, and Homeostasis by PTF1A.

Authors:  Chinh Q Hoang; Michael A Hale; Ana C Azevedo-Pouly; Hans P Elsässer; Tye G Deering; Spencer G Willet; Fong C Pan; Mark A Magnuson; Christopher V E Wright; Galvin H Swift; Raymond J MacDonald
Journal:  Mol Cell Biol       Date:  2016-11-28       Impact factor: 4.272

7.  p53 mutations cooperate with oncogenic Kras to promote adenocarcinoma from pancreatic ductal cells.

Authors:  J M Bailey; A M Hendley; K J Lafaro; M A Pruski; N C Jones; J Alsina; M Younes; A Maitra; F McAllister; C A Iacobuzio-Donahue; S D Leach
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8.  Complexity of molecular alterations impacts pancreatic cancer prognosis.

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Review 9.  Pancreatic cancer and its stroma: a conspiracy theory.

Authors:  Zhihong Xu; Srinivasa P Pothula; Jeremy S Wilson; Minoti V Apte
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10.  REG3A/REG3B promotes acinar to ductal metaplasia through binding to EXTL3 and activating the RAS-RAF-MEK-ERK signaling pathway.

Authors:  Huairong Zhang; Andrea Liliam Gomez Corredor; Julia Messina-Pacheco; Qing Li; George Zogopoulos; Nancy Kaddour; Yifan Wang; Bing-Yin Shi; Alex Gregorieff; Jun-Li Liu; Zu-Hua Gao
Journal:  Commun Biol       Date:  2021-06-07
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