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Pancreatic Cancer pp 577–599Cite as

Utility of Animal Models in Pancreatic Cancer Research

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Part of the book series: M. D. Anderson Solid Tumor Oncology Series ((MDA))

The vast majority of human pancreatic cancers (∼95%) are classified as ductal adenocarcinomas (1, 2), whereas acinar cell carcinomas and other histologic types are much less common. The cell origin of ductal adenocarcinomas is still under debate (3). Some studies have suggested that it arises from metaplasia (transdifferentiation) of acinar cells or even endocrine (islet) cells to ductal cells leading to ductal adenocarcinoma (3, 4) Although this has been based on cell lines and animal models, observations on human carcinomas, however, imply a different scenario. Hyperplastic and dysplastic epithelial lesions of the pancreatic ducts have been identified frequently in association with ductal adenocarcinomas (5), and these are now referred to as pancreatic intraepithelial neoplasia (PanINs) (6, 7). The evidence thus suggests that ductal adenocarcinomas may simply be originating from ductal cells, although it cannot be ruled out that ductal metaplasia of other cell types, especially acinar cells or centro-acinar cells (trans-differentiation or formation of ductular structures) could also be involved in the development of ductal adenocarcinoma under different situations, including genetic or epigenetic processes. Moreover, recent studies by Guerra et al. provided strong evidence for a role for pancreatic tissue damage and pancreatitis in the etiology of pancreatic ductal adenocarcinoma (PDAC) (9).

It is certain that the etiology of PDACs is fairly complex and poorly understood. This chapter provides an overview of the histologic and molecular complexities of pancreatic neoplasia as they apply to and correlate with different animal models, with a focus on transgenic mice and mice bearing human pancreatic tumor cells as xenografts, and their potential utility for developing preventive and/or therapeutic strategies.

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Authors and Affiliations

  1. Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan, USA

    Asfar S. Azmi PhD & Fazlul H. Sarkar PhD

  2. Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan, USA

    Mussop Mohammad BSc & Ramzi M. Mohammad BSc

  3. The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA

    Ahmed O. Kaseb MD

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  1. Asfar S. Azmi PhD
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Editors and Affiliations

  1. University of California San Diego, La Jolla, CA, USA

    Andrew M. Lowy

  2. School of Medicine, Johns Hopkins University, Baltimore, MD, USA

    Steven D. Leach

  3. Wayne State University, Detroit, MI, USA

    Philip A. Philip

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Azmi, A.S., Mohammad, M., Kaseb, A.O., Sarkar, F.H., Mohammad, R.M. (2008). Utility of Animal Models in Pancreatic Cancer Research. In: Lowy, A.M., Leach, S.D., Philip, P.A. (eds) Pancreatic Cancer. M. D. Anderson Solid Tumor Oncology Series. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-69252-4_34

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