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Review
. 2011 May 18:13:e18.
doi: 10.1017/S1462399411001876.

Oncolytic virotherapy for pancreatic cancer

Sonia Wennier  1 , Shoudong Li, Grant McFadden
Affiliations
Review

Oncolytic virotherapy for pancreatic cancer

Sonia Wennier et al. Expert Rev Mol Med. .

Abstract

Within the past decade, many oncolytic viruses (OVs) have been studied as potential treatments for pancreatic cancer and some of these are currently under clinical trials. The applicability of certain OVs, such as adenoviruses, herpesviruses and reoviruses, for the treatment of pancreatic cancer has been intensively studied for several years, whereas the applicability of other more recently investigated OVs, such as poxviruses and parvoviruses, is only starting to be determined. At the same time, studies have identified key characteristics of pancreatic cancer biology that provide a better understanding of the important factors or pathways involved in this disease. This review aims to summarise the different replication-competent OVs proposed as therapeutics for pancreatic cancer. It also focuses on the unique biology of these viruses that makes them exciting candidate virotherapies for pancreatic cancer and discusses how they could be genetically manipulated or combined with other drugs to improve their efficacy based on what is currently known about the molecular biology of pancreatic cancer.

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Figures

Figure 1
Figure 1. Specificity of oncolytic viruses for pancreatic cancer
Pancreatic cancer cells arise from normal ductal cells upon genetic alterations that lead to the dysregulation of specific signalling pathways. Oncolytic viruses (OVs) cannot replicate in normal cells owing to inefficient viral entry, induction of innate intracellular antiviral responses or an inadequate intracellular signalling environment. The specificity of OVs can be dictated at the step of viral entry or later, within the specific intracellular environment of the pancreatic cancer cell. Successful replication of an OV in the cancer cell should lead to oncolysis. Oncolysis can be achieved through several methods, which include, among others, the direct lysis of cancer cells as a product of lytic viral replication as well as the induction of a beneficial antitumour immune response triggered as a consequence of the activation of the immune reponse by the virus. Ultimately, virus is cleared by a protective antiviral immune response and tumour clearance can proceed by the establishment of the antitumour response.
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Further reading, resources and contacts

    1. Ottolino-Perry K, et al. Intelligent design: combination therapy with oncolytic viruses. Molecular Therapy. 2009;18:251–263. This review details combination therapies with OVs.

    1. Power AT, Bell JC. Taming the Trojan horse: optimizing dynamic carrier cell/oncolytic virus systems for cancer biotherapy. Gene Therapy. 2008;15:772–799. - PubMed

    1. Cattaneo R, et al. Reprogrammed viruses as cancer therapeutics: targeted, armed and shielded. Nature Reviews. Microbiology. 2008;6:529–540. These articles review cell-based delivery of OVs.

    1. Liu TC, Galanis E, Kirn D. Clinical trial results with oncolytic virotherapy: a century of promise, a decade of progress. Nature Clinical Practice. Oncology. 2007;4:101–117. These authors review clinical trials with OVs.

      For an overview of the frequent mutations found in the KRAS gene and other genes such as DCP4, P16 and P53 in pancreatic cancer, including cell line mutation profiles, see: http://pathology2.jhu.edu/pancreas/geneticsweb/discover.htm.

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