Chronic pancreatitis: a path to pancreatic cancer

Cancer Lett. 2014 Apr 10;345(2):203-9. doi: 10.1016/j.canlet.2013.08.015. Epub 2013 Aug 24.

Abstract

Chronic pancreatitis predisposes to pancreatic cancer development and both diseases share a common etiology. A central role has been proposed for the digestive enzyme-secreting acinar cell that can undergo ductal metaplasia in the inflammatory environment of pancreatitis. This metaplastic change is now a recognised precursor of pancreatic cancer. Inflammatory molecules also foster tumour growth through autocrine and paracrine effects in the epithelium and the stroma. These insights have raised new opportunities such as the manipulation of inflammation as a preventive and/or therapeutic strategy for pancreatic cancer. Finally, we address the need for an in-depth study of the pancreatic acinar cells.

Keywords: Acinar to ductal metaplasia; Dedifferentiation; Inflammation; Oxidative stress; Pancreatic cancer; Pancreatitis.

Publication types

  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Anticarcinogenic Agents / therapeutic use
  • Antineoplastic Agents / therapeutic use
  • Carcinoma, Pancreatic Ductal / drug therapy
  • Carcinoma, Pancreatic Ductal / etiology*
  • Carcinoma, Pancreatic Ductal / immunology
  • Carcinoma, Pancreatic Ductal / metabolism
  • Carcinoma, Pancreatic Ductal / prevention & control
  • Cell Transformation, Neoplastic / immunology
  • Cell Transformation, Neoplastic / metabolism
  • Humans
  • Inflammation Mediators / metabolism
  • Pancreatic Neoplasms / drug therapy
  • Pancreatic Neoplasms / etiology*
  • Pancreatic Neoplasms / immunology
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / prevention & control
  • Pancreatitis, Chronic / complications*
  • Pancreatitis, Chronic / drug therapy
  • Pancreatitis, Chronic / immunology
  • Pancreatitis, Chronic / metabolism
  • Risk Factors
  • Signal Transduction

Substances

  • Anti-Inflammatory Agents
  • Anticarcinogenic Agents
  • Antineoplastic Agents
  • Inflammation Mediators