Sugar pills for pancreatic cancer: The benefits of becoming (insulin) sensitive

doi:10.1053/gast.2001.23627

Gastroenterology

Volume 120, Issue 5, April 2001, Pages 1291-1296

https://doi.org/10.1053/gast.2001.23627 Get rights and content

Abstract

GASTROENTEROLOGY 2001;120:1291-1296

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Inflammation and the development of pancreatic cancer
2002, Surgical Oncology
Objective. Pancreatic cancer has an extremely poor prognosis and the cellular mechanisms contributing to pancreatic cancer are relatively unknown. The goals of this review are to present the epidemiological and experimental data that supports inflammation as a key mediator of pancreatic cancer development, to explain how inflammatory pathways may create an environment that supports tumor formation, and to discuss how the use of novel agents directed at these pathways may be used for the treatment of pancreatic malignancy. Summary Background Data. Inflammation has been identified as a significant factor in the development of other solid tumor malignancies. Both hereditary and sporadic forms of chronic pancreatitis are associated with an increased risk of developing pancreatic cancer. The combined increase in genomic damage and cellular proliferation, both of which are seen with inflammation, strongly favors malignant transformation of pancreatic cells. Cytokines, reactive oxygen species, and mediators of the inflammatory pathway (e.g., NF-κB and COX-2) have been shown to increase cell cycling, cause loss of tumor suppressor function, and stimulate oncogene expression; all of which may lead to pancreatic malignancy. Anti-cytokine vaccines, inhibitors of pro-inflammatory NF-κB and COX-2 pathways, thiazolidinediones, and anti-oxidants are potentially useful for the prevention or treatment of pancreatic cancer. Redirection of experimental interests toward pancreatic inflammation and mechanisms of carcinogenesis may identify other novel anti-inflammatory agents or other ways to screen for or prevent pancreatic cancer. Conclusion. Pancreatic inflammation, mediated by cytokines, reactive oxygen species, and upregulated pro-inflammatory pathways, may play a key role in the early development of pancreatic malignancy.
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^☆: Address requests for reprints to: Anna Mae Diehl, M.D., The Johns Hopkins University, 912 Ross Building, 720 Rutland Street, Baltimore, Maryland 21205. e-mail: [email protected]; fax: (410) 955-9677.

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EditorialsSugar pills for pancreatic cancer: The benefits of becoming (insulin) sensitive☆

Abstract

Gastroenterology

Gastroenterology

Biochem Biophys Res Commun

Biochem Biophys Res Commun

Immunobiology

J Biol Chem

Immunity

Curr Opin Cell Biol

Semin Cancer Biol

Surgery

A case-control study of diabetes mellitus and cancer risk

Br J Cancer

Implications of the hyperinsulinaemia-diabetes-cancer link for preventive efforts

Eur J Cancer Prev

Pancreatic neoplasms in an animal model: morphological, biological, and comparative studies

Cancer

Islet cells as a component of pancreatic ductal neoplasms. I. Experimental study: ductular cells, including islet cells precursors, as primary progenitor cells of tumors

Am J Pathol

Experimental evidence for the origin of ductal-type adenocarcinoma from the islets of Langerhans

Am J Pathol

Induction of adenocarcinoma from hamster pancreatic islet cells treated with N-nitrobis(2-oxopropyl)amine in vitro

Carcinogenesis

Overexpression of transforming growth factor-alpha: an epidermal growth factor receptor, but not epidermal growth factor, in exocrine pancreatic tumours in hamsters

Carcinogenesis

Establishment of tumor cell culture (ILA) derived from hamster pancreatic islets treated with BOP

Int J Cancer

Diabetes and pancreatic tumours in transgenic mice expression Pa x6

Diabetologia

Non-insulin-dependent diabetes mellitus: a genetically programmed failure of the beta cell to compensate for insulin resistance

N Engl J Med

Cellular mechanisms of insulin resistance in humans

Am J Cardiol

Pathophysiology of type 2 diabetes and modes of action of therapeutic interventions

Arch Intern Med

The antihyperglycaemic effect of metformin: therapeutic and cellular mechanisms

Drugs

Role of glucosamine pathway in fat-induced insulin resistance

J Clin Invest

Localization of the O-linked N-acetylglucosamine transferase in rat pancreas

Diabetes

Augmentation of UCP-GalNac: fucalpha1-2Gal alpha1-3 N-acetylgalactosaminyl transferase activity in nitrosamine-induced hamster pancreatic cancers

J Exp Clin Cancer Res

Editorials
Sugar pills for pancreatic cancer: The benefits of becoming (insulin) sensitive☆