Evidence map›Paper›PMID 27561180›Full record

ArticleCancer science2016

Measles virus selectively blind to signaling lymphocyte activity molecule has oncolytic efficacy against nectin-4-expressing pancreatic cancer cells.

Mutsumi Awano, Tomoko Fujiyuki, Koichiro Shoji, Yosuke Amagai, Yoshinori Murakami, Yoichi Furukawa, Hiroki Sato, Misako Yoneda, Chieko Kai

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

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  12. Article
  13. Therapeutic Applications for Oncolytic Self-Replicating RNA Viruses.International journal of molecular sciences · 2022
    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

9 authors.

Mutsumi AwanoLaboratory Animal Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Tomoko FujiyukiLaboratory Animal Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Koichiro ShojiLaboratory Animal Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yosuke AmagaiLaboratory Animal Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yoshinori MurakamiDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yoichi FurukawaClinical Genome Research, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Hiroki SatoLaboratory Animal Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Misako YonedaLaboratory Animal Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Chieko KaiLaboratory Animal Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer is one of the most intractable cancers and has a devastating prognosis; over the past three decades the 5-year survival rate has been <10%. Therefore, development of a novel anticancer treatment for pancreatic cancer is a matter of urgency. We previously developed an oncolytic recombinant measles virus (MV), rMV-SLAMblind, that had lost the ability to bind to its principal receptor, signaling lymphocyte activity molecule (SLAM), but which selectively infected and efficiently killed nectin-4-expressing breast and lung cancer cells. In this study, we analyzed the antitumor effect of this virus against pancreatic cancer. Nectin-4 was expressed on the surface of 4/16 tested pancreatic cancer cell lines, which were efficiently infected and killed by rMV-SLAMblind in vitro. The intratumoral inoculation of rMV-SLAMblind suppressed the growth of KLM1 and Capan-2 cells xenografted in SCID mice. The sequence analysis of MV isolated from the tumor revealed that the designed mutation in the H protein of rMV-SLAMblind had been stably maintained for 47 days after the last inoculation. These results suggest that rMV-SLAMblind is a promising candidate for the novel treatment of pancreatic cancer.

Indexed as

Signal TransductionAnimalsCell Adhesion MoleculesCell Line, TumorFemaleHumansLymphocytesMeasles virusMiceMice, SCIDNectinsOncolytic VirotherapyPancreatic NeoplasmsXenograft Model Antitumor AssaysCell Adhesion MoleculesNECTIN4 protein, humanNectinsMeasles virusnectin-4/PVRL4oncolytic virus therapypancreatic cancerxenograft

Identifiers

PMID27561180
PMCPMC5132336

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.