Evidence map›Paper›PMID 26085940›Full record

ArticleActa naturae

Mechanisms of Oncolysis by Paramyxovirus Sendai.

O V Matveeva, G V Kochneva, S V Netesov, S B Onikienko, P M Chumakov

Open access · bronzeAbstract read
In one paragraph

Article in Acta naturae. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. [Programmed cell death in paramyxovirus infection].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
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  12. Syncytia Formation in Oncolytic Virotherapy.Molecular therapy oncolytics · 2019
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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

5 authors at 4 institutions in 1 country.

O V MatveevaBiopolymer Design, 23 Nylander Way, Acton, Massachusetts, United States.
G V KochnevaCenter of Virology and Biotechnology "Vector", Koltsovo, Novosibirsk Region, Russia.
S V NetesovNovosibirsk State University, Novosibirsk, Russia.
S B OnikienkoDepartment of Military Field Therapy, Kirov Military Medical Academy, St. Petersburg, Russia.
P M ChumakovEngelhardt Institute of Molecular Biology, Moscow, Russia.
Engelhardt Institute of Molecular Biology · RUNovosibirsk State University · RUS. M. Kirov Military Medical Academy · RUState Research Center of Virology and Biotechnology VECTOR · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Some viral strains of the Paramyxoviridae family may be used as anti-tumor agents. Oncolytic paramyxoviruses include attenuated strains of the measles virus, Newcastle disease virus, and Sendai virus. These viral strains, and the Sendai virus in particular, can preferentially induce the death of malignant, rather than normal, cells. The death of cancer cells results from both direct killing by the virus and through virus-induced activation of anticancer immunity. Sialic-acid-containing glycoproteins that are overexpressed in cancer cells serve as receptors for some oncolytic paramyxoviruses and ensure preferential interaction of paramyxoviruses with malignant cells. Frequent genetic defects in interferon and apoptotic response systems that are common to cancer cells ensure better susceptibility of malignant cells to viruses. The Sendai virus as a Paramyxovirus is capable of inducing the formation of syncytia, multinuclear cell structures which promote viral infection spread within a tumor without virus exposure to host neutralizing antibodies. As a result, the Sendai virus can cause mass killing of malignant cells and tumor destruction. Oncolytic paramyxoviruses can also promote the immune-mediated elimination of malignant cells. In particular, they are powerful inducers of interferon and other cytokynes promoting antitumor activity of various cell components of the immune response, such as dendritic and natural killer cells, as well as cytotoxic T lymphocytes. Taken together these mechanisms explain the impressive oncolytic activity of paramyxoviruses that hold promise as future, efficient anticancer therapeutics.

Indexed as

attenuated measles virus strainscancer therapyNewcastle disease virusoncolytic paramyxovirusesSendai virusviral anticancer immune stimulationviral anti-tumor mechanism

Identifiers

PMID26085940
PMCPMC4463408
OpenAlexW1778227654

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.