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Pancreatic Cancer and Diabetes

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Diabetes

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 771))

Abstract

Diabetes studies have increasingly been associated with several types of cancer. Diabetes and pancreatic cancer have a unique relationship. Genetic mutations, such as activation of the KRAS2 oncogene, inactivation of the tumor-suppressor gene CDKN2A, inactivation of the tumor-suppressor gene TP53 and deleted in pancreatic cancer 4 (DPC4) gene defects are seen in those with pancreatic cancer. Approximately 80%of those patients, diagnosed with pancreatic cancer, are identified as having concomitant diabetes with a poor prognostic factor. Damaged pancreatic tissue, secondary to pancreatic cancer, leads to diabetes as islet cells and β cells are taken over by malignancy. Additionally, those on certain anti-diabetic regimens are shown to be at a higher risk of developing pancreatic cancer due to the effect of stimulation on the pancreatic β and islet cells. Therefore, diabetes is thought to be both a potential cause and effect of pancreatic cancer. Diabetes has become a pandemic, and pancreatic cancer is one of the most lethal forms of malignancy known. In order to better understand these diseases and how they are associated, more research needs to be done. Particularly, research focusing on different types of diabetes in the setting of pancreatic cancer will be an important issue for further understanding of the link between diabetes and pancreatic cancer.

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Author information

Authors and Affiliations

  1. Swedish Organ Transplant Division, Swedish Medical Center, Seattle, Washington, USA

    Maureen Morrison

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  1. Maureen Morrison
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Editor information

Editors and Affiliations

  1. School of Science and Technology, Nottingham Trent University, Nottingham, UK

    Shamim I. Ahmad BSc, MSc, PhD

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© 2013 Landes Bioscience and Springer Science+Business Media

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Morrison, M. (2013). Pancreatic Cancer and Diabetes. In: Ahmad, S.I. (eds) Diabetes. Advances in Experimental Medicine and Biology, vol 771. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-5441-0_18

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