Evidence map›Paper›PMID 19180240›Full record

ArticlePloS one2009

Towards predictive computational models of oncolytic virus therapy: basis for experimental validation and model selection.

Dominik Wodarz, Natalia Komarova

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
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  9. Review
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  11. Review
  12. Article
  13. Article
  14. The Role of the Innate Immune System in Oncolytic Virotherapy.Computational and mathematical methods in medicine · 2017
    Article
  15. Computational modeling approaches to the dynamics of oncolytic viruses.Wiley interdisciplinary reviews. Systems biology and medicine · 2016
    Review
  16. Article
  17. Perfusion Pressure Is a Critical Determinant of the Intratumoral Extravasation of Oncolytic Viruses.Molecular therapy : the journal of the American Society of Gene Therapy · 2016
    Article
  18. Article
  19. Modeling T cell responses to antigenic challenge.Journal of pharmacokinetics and pharmacodynamics · 2014
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Dominik WodarzDepartment of Ecology and Evolution, University of California Irvine, Irvine, California, United States of America. dwodarz@uci.edu
Natalia Komarova
University of California, Irvine · US

Funding

Mathematical Models of Programmed CTL ProliferationR01AI058153 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI WODARZ, DOMINIK F · 2005 to 2009
$530k
NIAID NIH HHS 1R01AI058153-04NIAID NIH HHS R01 AI058153
6 · The paper itself

Abstract

Oncolytic viruses are viruses that specifically infect cancer cells and kill them, while leaving healthy cells largely intact. Their ability to spread through the tumor makes them an attractive therapy approach. While promising results have been observed in clinical trials, solid success remains elusive since we lack understanding of the basic principles that govern the dynamical interactions between the virus and the cancer. In this respect, computational models can help experimental research at optimizing treatment regimes. Although preliminary mathematical work has been performed, this suffers from the fact that individual models are largely arbitrary and based on biologically uncertain assumptions. Here, we present a general framework to study the dynamics of oncolytic viruses that is independent of uncertain and arbitrary mathematical formulations. We find two categories of dynamics, depending on the assumptions about spatial constraints that govern that spread of the virus from cell to cell. If infected cells are mixed among uninfected cells, there exists a viral replication rate threshold beyond which tumor control is the only outcome. On the other hand, if infected cells are clustered together (e.g. in a solid tumor), then we observe more complicated dynamics in which the outcome of therapy might go either way, depending on the initial number of cells and viruses. We fit our models to previously published experimental data and discuss aspects of model validation, selection, and experimental design. This framework can be used as a basis for model selection and validation in the context of future, more detailed experimental studies. It can further serve as the basis for future, more complex models that take into account other clinically relevant factors such as immune responses.

Indexed as

Oncolytic VirotherapyVirus ReplicationAdenoviridaeAnimalsCell Line, TumorHumansMiceMice, NudeModels, BiologicalNeoplasmsOncolytic Viruses

Identifiers

PMID19180240
PMCPMC2629569
OpenAlexW1964809585

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.