Induction of Pancreatic Inflammation Accelerates Pancreatic Tumorigenesis in Mice

Methods Mol Biol. 2019:1882:287-297. doi: 10.1007/978-1-4939-8879-2_25.

Abstract

Pancreatitis is a major risk factor for the development of pancreatic cancer. In genetically engineered mouse models, induction of pancreatic inflammation dramatically accelerates oncogenic KRas-induced fibrosis, precancerous PanIN formation, and tumorigenesis. Here we describe simple methods of secretagogue-induced experimental acute and chronic pancreatitis, the most commonly used pancreatitis models, and their applications in pancreatic cancer research. Additionally, the preparation of primary pancreatic acinar cells is introduced. Primary acinar cells can be used to study the early events of pancreatic inflammation and pancreatic acinar-to-ductal (ADM) metaplasia.

Keywords: Acinar cell; CCK; Caerulein; KRas; Pancreatic cancer; Pancreatitis.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Acinar Cells / pathology
  • Animals
  • Carcinogenesis / chemically induced
  • Carcinogenesis / genetics
  • Cell Transformation, Neoplastic / chemically induced
  • Cell Transformation, Neoplastic / genetics
  • Ceruletide / toxicity
  • Disease Models, Animal
  • Humans
  • Metaplasia / chemically induced
  • Metaplasia / pathology
  • Mice
  • Mice, Transgenic
  • Mutation
  • Pancreas / cytology
  • Pancreas / pathology*
  • Pancreatic Ducts / cytology
  • Pancreatic Ducts / pathology
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / pathology*
  • Pancreatitis / chemically induced
  • Pancreatitis / pathology*
  • Primary Cell Culture / instrumentation
  • Primary Cell Culture / methods*
  • Proto-Oncogene Proteins p21(ras) / genetics
  • Tumor Cells, Cultured

Substances

  • Ceruletide
  • Hras protein, mouse
  • Proto-Oncogene Proteins p21(ras)