Evidence map›Paper›PMID 28695108›Full record

ArticleFrontiers in oncology2017

Enhancing the Oncolytic Activity of CD133-Targeted Measles Virus: Receptor Extension or Chimerism with Vesicular Stomatitis Virus Are Most Effective.

Dina Kleinlützum, Julia D S Hanauer, Alexander Muik, Kay-Martin Hanschmann, Sarah-Katharina Kays, Camilo Ayala-Breton, Kah-Whye Peng, Michael D Mühlebach, Tobias Abel, Christian J Buchholz

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  8. CD90-targeted lentiviral vectors for HSC gene therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  9. Review
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  11. Review
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  13. Article
  14. Syncytia Formation in Oncolytic Virotherapy.Molecular therapy oncolytics · 2019
    Review
  15. Article
  16. Article
  17. Review
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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 3 institutions in 2 countries.

Dina KleinlützumMolecular Biotechnology and Gene Therapy, Paul-Ehrlich-Institut, Langen, Germany.
Julia D S HanauerMolecular Biotechnology and Gene Therapy, Paul-Ehrlich-Institut, Langen, Germany.
Alexander MuikMolecular Biotechnology and Gene Therapy, Paul-Ehrlich-Institut, Langen, Germany.
Kay-Martin HanschmannBiostatistics, Paul-Ehrlich-Institut, Langen, Germany.
Sarah-Katharina KaysMolecular Biotechnology and Gene Therapy, Paul-Ehrlich-Institut, Langen, Germany.
Camilo Ayala-BretonDepartment of Molecular Medicine, Mayo Clinic, Rochester, MN, United States.
Kah-Whye PengDepartment of Molecular Medicine, Mayo Clinic, Rochester, MN, United States.
Michael D MühlebachProduct Testing of Immunological Medicinal Products for Veterinary Use, Paul-Ehrlich-Institut, Langen, Germany.
Tobias AbelMolecular Biotechnology and Gene Therapy, Paul-Ehrlich-Institut, Langen, Germany.
Christian J BuchholzMolecular Biotechnology and Gene Therapy, Paul-Ehrlich-Institut, Langen, Germany.
Paul Ehrlich Institut · DEMayo Clinic in Arizona · USDeutschen Konsortium für Translationale Krebsforschung · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Therapy resistance and tumor recurrence are often linked to a small refractory and highly tumorigenic subpopulation of neoplastic cells, known as cancer stem cells (CSCs). A putative marker of CSCs is CD133 (prominin-1). We have previously described a CD133-targeted oncolytic measles virus (MV-CD133) as a promising approach to specifically eliminate CD133-positive tumor cells. Selectivity was introduced at the level of cell entry by an engineered MV hemagglutinin (H). The H protein was blinded for its native receptors and displayed a CD133-specific single-chain antibody fragment (scFv) as targeting domain. Interestingly, MV-CD133 was more active in killing CD133-positive tumors than the unmodified MV-NSe despite being highly selective for its target cells. To further enhance the antitumoral activity of MV-CD133, we here pursued arming technologies, receptor extension, and chimeras between MV-CD133 and vesicular stomatitis virus (VSV). All newly generated viruses including VSV-CD133 were highly selective in eliminating CD133-positive cells. MV-CD46/CD133 killed in addition CD133-negative cells being positive for the MV receptors. In an orthotopic glioma model, MV-CD46/CD133 and MV

Indexed as

glioblastomahepatocellular carcinomaprominin-1tumorspherevirotherapy

Identifiers

PMID28695108
PMCPMC5483446
OpenAlexW2711147957

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.