Armed oncolytic viruses: A kick-start for anti-tumor immunity

[Display omitted] •Oncolytic viruses expressing immune modulators as transgene enhance the efficacy of anti-tumor therapies.•The enhanced efficacy is dependent on the combination of virus and immune modulator.•The localized expression of transgenic agonistic agents could reduce adverse effects in co...

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Published inCytokine & growth factor reviews Vol. 41; pp. 28 - 39
Main Authors de Graaf, J.F., de Vor, L., Fouchier, R.A.M., van den Hoogen, B.G.
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.06.2018
The Authors. Published by Elsevier Ltd
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Summary:[Display omitted] •Oncolytic viruses expressing immune modulators as transgene enhance the efficacy of anti-tumor therapies.•The enhanced efficacy is dependent on the combination of virus and immune modulator.•The localized expression of transgenic agonistic agents could reduce adverse effects in contrast to systemic administration.•Arming viruses with checkpoint inhibitors might not be the most effective combination strategy compared to agonistic agents. Oncolytic viruses (OVs), viruses that specifically result in killing tumor cells, represent a promising class of cancer therapy. Recently, the focus in the OV therapy field has shifted from their direct oncolytic effect to their immune stimulatory effect. OV therapy can function as a “kick start” for the antitumor immune response by releasing tumor associated antigens and release of inflammatory signals. Combining OVs with immune modulators could enhance the efficacy of both immune and OV therapies. Additionally, genetic engineering of OVs allows local expression of immune therapeutics, thereby reducing related toxicities. Different options to modify the tumor microenvironment in combination with OV therapy have been explored. The possibilities and obstacles of these combinations will be discussed in this review.
Bibliography:Present address: Department of Microbiology, UMC, Utrecht, The Netherlands.
ISSN:1359-6101
1879-0305
DOI:10.1016/j.cytogfr.2018.03.006