Evidence map›Paper›PMID 20606645›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2010

Urokinase-targeted fusion by oncolytic Sendai virus eradicates orthotopic glioblastomas by pronounced synergy with interferon-β gene.

Yuzo Hasegawa, Hiroaki Kinoh, Yasuo Iwadate, Mitsuho Onimaru, Yasuji Ueda, Yui Harada, Satoru Saito, Aki Furuya, Takashi Saegusa, Yosuke Morodomi and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Gene Therapy and Cardiovascular Diseases.Advances in experimental medicine and biology · 2023
    Article
  2. Review
  3. Review
  4. Article
  5. Syncytia Formation in Oncolytic Virotherapy.Molecular therapy oncolytics · 2019
    Review
  6. Article
  7. Viral and Synthetic RNA Vector Technologies and Applications.Molecular therapy : the journal of the American Society of Gene Therapy · 2016
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Recent advances in oncolytic virus design.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2011
    Review
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

15 authors at 4 institutions in 1 country.

Yuzo HasegawaDepartment of Neurological Surgery, Chiba University Graduate School of Medicine, Chiba, Japan.
Hiroaki Kinoh
Yasuo Iwadate
Mitsuho Onimaru
Yasuji Ueda
Yui Harada
Satoru Saito
Aki Furuya
Takashi Saegusa
Yosuke Morodomi
Mamoru Hasegawa
Shigeyoshi Saito
Ichio Aoki
Naokatsu Saeki
Yoshikazu Yonemitsu
Kyushu University · JPID Pharma (Japan) · JPChiba University · JPChiba Rosai Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GM), the most frequent primary malignant brain tumor, is highly invasive due to the expression of proteases, including urokinase-type plasminogen activator (uPA). Here, we show the potential of our new and powerful recombinant Sendai virus (rSeV) showing uPA-specific cell-to-cell fusion activity [rSeV/dMFct14 (uPA2), named "BioKnife"] for GM treatment, an effect that was synergistically enhanced by arming BioKnife with the interferon-β (IFN-β) gene. BioKnife killed human GM cell lines efficiently in a uPA-dependent fashion, and this killing was prevented by PA inhibitor-1. Rat gliosarcoma 9L cells expressing both uPA and its functional receptor uPAR (9L-L/R) exhibited high uPA activity on the cellular surface and were highly susceptible to BioKnife. Although parent 9L cells (9L-P) were resistant to BioKnife and to BioKnife expressing IFN-β (BioKnife-IFNβ), cell-cell fusion of 9L-L/R strongly facilitated the expression of IFN-β, and in turn, IFN-β significantly accelerated the fusion activity of BioKnife. A similar synergy was seen in a rat orthotopic brain GM model with 9L-L/R in vivo; therefore, these results suggest that BioKnife-IFNβ may have significant potential to improve the survival of GM patients in a clinical setting.

Indexed as

AnimalsBlotting, WesternCell LineCell Line, TumorCell SurvivalEnzyme-Linked Immunosorbent AssayFemaleGlioblastomaHumansInterferon-betaMagnetic Resonance ImagingMiceMice, NudeOncolytic VirusesPlasminogen Activator Inhibitor 1RatsInterferon-betaPlasminogen Activator Inhibitor 1Receptors, Urokinase Plasminogen ActivatorUrokinase-Type Plasminogen Activator

Identifiers

PMID20606645
PMCPMC2951556
OpenAlexW2004534033

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.