ArticleJournal of the Royal Society, Interface2009
Use of oncolytic viruses for the eradication of drug-resistant cancer cells.
Article in Journal of the Royal Society, Interface, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Phase I/II study of oncolytic herpes simplex virus NV1020 in patients with extensively pretreated refractory colorectal cancer metastatic to the liver.Human gene therapy · 2010Trial
- Oncolytic Viruses and Hematological Malignancies: A New Class of Immunotherapy Drugs.Current oncology (Toronto, Ont.) · 2020Review
- Virus-Receptor Interactions and Virus Neutralization: Insights for Oncolytic Virus Development.Oncolytic virotherapy · 2020Review
- In vitro and in silico multidimensional modeling of oncolytic tumor virotherapy dynamics.PLoS computational biology · 2019Article
- Oncolytic virotherapy for urological cancers.Nature reviews. Urology · 2016Review
- Computational modeling approaches to the dynamics of oncolytic viruses.Wiley interdisciplinary reviews. Systems biology and medicine · 2016Review
- Complex spatial dynamics of oncolytic viruses in vitro: mathematical and experimental approaches.PLoS computational biology · 2012Article
Corrections and comments
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Authors and funding
1 author.
Funding
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Abstract
Targeted therapy using small-molecule inhibitors is a promising new therapy approach against cancer, but drug-resistant mutants present an obstacle to success. Oncolytic virus therapy, where viruses replicate specifically in cancer cells and kill them, is another promising therapy approach against cancer. While encouraging results have been observed in clinical trials, consistent success has not been possible so far. Based on a computational framework, I report that even if oncolytic virus therapy fails to eradicate a cancer, it can have the potential to eradicate the sub-population of drug-resistant cancer cells. Once this has occurred, targeted drug therapy can be used to induce cancer remission. For this to work, a drug resistance mutation must confer a certain fitness cost to the cell, as has been documented in the literature. The reason for this finding is that in the presence of a shared virus, the faster growing (drug-sensitive) cell population produces an amount of virus that is too much for the slower growing (drug-resistant) cell population to survive. This is derived from a population dynamic principle known as apparent competition. Therefore, a sequential combination of oncolytic virus and targeted therapies can overcome major weaknesses of either approach alone.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.