Evidence map›Paper›PMID 28578991›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2017

Oncolytic VSV Primes Differential Responses to Immuno-oncology Therapy.

Nicholas M Durham, Kathy Mulgrew, Kelly McGlinchey, Noel R Monks, Hong Ji, Ronald Herbst, JoAnn Suzich, Scott A Hammond, Elizabeth J Kelly

Open access · hybridAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Nicholas M DurhamMedImmune, LLC, One Medimmune Way, Gaithersburg, MD 20878, USA.
Kathy MulgrewMedImmune, LLC, One Medimmune Way, Gaithersburg, MD 20878, USA.
Kelly McGlincheyMedImmune, LLC, One Medimmune Way, Gaithersburg, MD 20878, USA.
Noel R MonksMedImmune, LLC, One Medimmune Way, Gaithersburg, MD 20878, USA.
Hong JiMedImmune, LLC, One Medimmune Way, Gaithersburg, MD 20878, USA.
Ronald HerbstMedImmune, LLC, One Medimmune Way, Gaithersburg, MD 20878, USA.
JoAnn SuzichMedImmune, LLC, One Medimmune Way, Gaithersburg, MD 20878, USA.
Scott A HammondMedImmune, LLC, One Medimmune Way, Gaithersburg, MD 20878, USA.
Elizabeth J KellyMedImmune, LLC, One Medimmune Way, Gaithersburg, MD 20878, USA. Electronic address: kellybe@medimmune.com.
Altimmune (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vesicular stomatitis virus encoding the IFNβ transgene (VSV-IFNβ) is a mediator of potent oncolytic activity and is undergoing clinical evaluation for the treatment of solid tumors. Emerging preclinical and clinical data suggest treatment of tumors with oncolytic viruses may sensitize tumors to checkpoint inhibitors and increase the anti-tumor immune response. New generations of immuno-oncology molecules including T cell agonists are entering clinical development and could be hypothesized to enhance the activity of oncolytic viruses, including VSV-IFNβ. Here, we show that VSV-IFNβ exhibits multiple mechanisms of action, including direct cell killing, stimulation of an innate immune response, recruitment of CD8 T cells, and depletion of T regulatory cells. Moreover, VSV-IFNβ promotes the establishment of a CD8 T cell response to endogenous tumor antigens. Our data demonstrate a significant enhancement of anti-tumor function for VSV-IFNβ when combined with checkpoint inhibitors, but not OX40 agonists. While the addition of checkpoint inhibitors to VSV-IFNβ generated robust tumor growth inhibition, it resulted in no increase in viral replication, transgene expression, or immunophenotypic changes beyond treatment with VSV-IFNβ alone. We hypothesize that tumor-specific T cells generated by VSV-IFNβ retain activity due to a lack of immune exhaustion when checkpoint inhibitors were used.

Indexed as

Genetic TherapyImmunotherapyOncolytic VirotherapyAnimalsAntibodies, MonoclonalB7-H1 AntigenBiomarkers, TumorCombined Modality TherapyDisease Models, AnimalGene ExpressionGenetic VectorsHumansImmunomodulationInterferon-betaInterferonsMelanoma, ExperimentalAntibodies, MonoclonalB7-H1 AntigenBiomarkers, TumorCD274 protein, humanInterferon-betaInterferonsReceptors, OX40agonistcheckpoint inhibitorimmune-oncologyoncolytic virusVSV

Identifiers

PMID28578991
PMCPMC5542805
OpenAlexW2613044804

What OpenQuestion holds

Textmetadata
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.