Evidence map›Paper›PMID 18533893›Full record

ArticleHuman gene therapy2008

rVSV(M Delta 51)-M3 is an effective and safe oncolytic virus for cancer therapy.

Lan Wu, Tian-gui Huang, Marcia Meseck, Jennifer Altomonte, Oliver Ebert, Katsunori Shinozaki, Adolfo García-Sastre, John Fallon, John Mandeli, Savio L C Woo

Open access · greenAbstract read
In one paragraph

Article in Human gene therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

49 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
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  6. Repurposing the oncolytic virus VSV∆51M as a COVID-19 vaccine.Frontiers in bioengineering and biotechnology · 2023
    Article
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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

10 authors at 1 institution in 1 country.

Lan WuDepartment of Gene and Cell Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.
Tian-gui Huang
Marcia Meseck
Jennifer Altomonte
Oliver Ebert
Katsunori Shinozaki
Adolfo García-Sastre
John Fallon
John Mandeli
Savio L C Woo
Icahn School of Medicine at Mount Sinai · US

Funding

VIRULENCE FACTORS OF INFLUENZA VIRUS--THE NS1 PROTEINR01AI046954 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GARCIA-SASTRE, ADOLFO · 2000 to 2010
$3.1M
Onoclytic VSV for Hepatocellular CarcinomaR01CA100830 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI WOO, SAVIO L · 2003 to 2011
$3.0M
NCI NIH HHS CA100830NCI NIH HHS R01 CA100830NIAID NIH HHS R01 AI046954
6 · The paper itself

Abstract

Oncolytic vesicular stomatitis virus (VSV) is being developed as a novel therapeutic agent for cancer treatment, although it is toxic in animals when administered systemically at high doses. Its safety can be substantively improved by an M Delta 51 deletion in the viral genome, and yet VSV(M Delta 51) induces a much greater, robust cellular inflammatory response in the host than wild-type VSV, which severely attenuates its oncolytic potency. We have reported that the oncolytic potency of wild-type VSV can be enhanced by vector-mediated expression of a heterologous viral gene that suppresses cellular inflammatory responses in the lesions. To develop an effective and safe VSV vector for cancer treatment, we tested the hypothesis that the oncolytic potency of VSV(M Delta 51) can be substantively elevated by vector-mediated expression of M3, a broad-spectrum and high-affinity chemokine-binding protein from murine gammaherpesvirus-68. The recombinant vector rVSV(M Delta 51)-M3 was used to treat rats bearing multifocal lesions (1-10 mm in diameter) of hepatocellular carcinoma (HCC) in their liver by hepatic artery infusion. Treatment led to a significant reduction of neutrophil and natural killer cell accumulation in the lesions, a 2-log elevation of intratumoral viral titer, substantively enhanced tumor necrosis, and prolonged animal survival with a 50% cure rate. Importantly, there were no apparent systemic and organ toxicities in the treated animals. These results indicate that the robust cellular inflammatory responses induced by VSV(M Delta 51) in HCC lesions can be overcome by vector-mediated intratumoral M3 expression, and that rVSV(M Delta 51)-M3 can be developed as an effective and safe oncolytic agent to treat advanced HCC patients in the future.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorCell SurvivalCytokinesGenetic VectorsKiller Cells, NaturalLeukocyte Reduction ProceduresLiver NeoplasmsLymphocyte DepletionMaleNeutrophilsOncolytic VirotherapyOncolytic VirusesRatsRats, Inbred BUFCytokinesM3 protein, Murine gammaherpesvirusViral Proteins

Identifiers

PMID18533893
PMCPMC2775926
OpenAlexW2131132108

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.