Evidence map›Paper›PMID 28797937›Full record

ArticleTranslational oncology2017

Immunohistochemical Characterization and Sensitivity to Human Adenovirus Serotypes 3, 5, and 11p of New Cell Lines Derived from Human Diffuse Grade II to IV Gliomas.

Minna Niittykoski, Mikael von Und Zu Fraunberg, Miika Martikainen, Tuomas Rauramaa, Arto Immonen, Susanna Koponen, Ville Leinonen, Markus Vähä-Koskela, Qiwei Zhang, Florian Kühnel and 4 more

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.2field-weighted citation impact, top 33% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

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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

14 authors at 7 institutions in 4 countries.

Minna NiittykoskiBiotechnology and Molecular Medicine, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland. Electronic address: mijoni@gmail.com.
Mikael von Und Zu FraunbergNeuroCenter of Kuopio University Hospital, Kuopio, Finland; Neurosurgery, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland. Electronic address: mikael.fraunberg@kuh.fi.
Miika MartikainenBiotechnology and Molecular Medicine, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland; Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden. Electronic address: miika.martikainen@igp.uu.se.
Tuomas RauramaaPathology, Institute of Clinical Medicine, University of Eastern Finland and Department of Pathology, Kuopio University Hospital, Kuopio, Finland. Electronic address: tuomas.rauramaa@uef.fi.
Arto ImmonenNeuroCenter of Kuopio University Hospital, Kuopio, Finland; Neurosurgery, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland. Electronic address: arto.immonen@kuh.fi.
Susanna KoponenNeuroCenter of Kuopio University Hospital, Kuopio, Finland. Electronic address: susanna.koponen@kuh.fi.
Ville LeinonenNeuroCenter of Kuopio University Hospital, Kuopio, Finland; Neurosurgery, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland. Electronic address: ville.leinonen@kuh.fi.
Markus Vähä-KoskelaInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland. Electronic address: markus.vaha-koskela@helsinki.fi.
Qiwei ZhangSouthern Medical University, Guangzhou, Guangdong, China. Electronic address: Zhang.Qiwei@yahoo.com.
Florian KühnelDepartment of Gastroenterology, Hepatology and Endocrinology, Medical School, Hannover, Germany. Electronic address: kuehnel.florian@mh-hannover.de.
Ya-Fang MeiDepartment of Clinical Microbiology, Umeå University, Umeå, Sweden. Electronic address: ya-fang.mei@umu.se.
Seppo Ylä-HerttualaBiotechnology and Molecular Medicine, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland. Electronic address: seppo.ylaherttuala@uef.fi.
Juha E JääskeläinenNeuroCenter of Kuopio University Hospital, Kuopio, Finland; Neurosurgery, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland. Electronic address: juha.e.jaaskelainen@kuh.fi.
Ari HinkkanenBiotechnology and Molecular Medicine, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland. Electronic address: ari.hinkkanen@utu.fi.
University of Eastern Finland · FIKuopio University Hospital · FIInstitute for Molecular Medicine Finland · FIMedizinische Hochschule Hannover · DEScience for Life Laboratory · SESouthern Medical University · CNUmeå University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOncolytic adenoviruses show promise in targeting gliomas because they do not replicate in normal brain cells. However, clinical responses occur only in a subset of patients. One explanation could be the heterogenic expression level of virus receptors. Another contributing factor could be variable activity of tumor antiviral defenses in different glioma subtypes.

methodsWe established a collection of primary low-passage cell lines from different glioma subtypes (3 glioblastomas, 3 oligoastrocytomas, and 2 oligodendrogliomas) and assessed them for receptor expression and sensitivity to human adenovirus (HAd) serotypes 3, 5, and 11p. To gauge the impact of antiviral defenses, we also compared the infectivity of the oncolytic adenoviruses in interferon (IFN)-pretreated cells with IFN-sensitive Semliki Forest virus (SFV).

resultsImmunostaining revealed generally low expression of HAd5 receptor CAR in both primary tumors and derived cell lines. HAd11p receptor CD46 levels were maintained at moderate levels in both primary tumor samples and derived cell lines. HAd3 receptor DSG-2 was reduced in the cell lines compared to the tumors. Yet, at equal multiplicities of infection, the oncolytic potency of HAd5 in vitro in tumor-derived cells was comparable to HAd11p, whereas HAd3 lysed fewer cells than either of the other two HAd serotypes in 72 hours. IFN blocked replication of SFV, while HAds were rather unaffected.

conclusionsAdenovirus receptor levels on glioma-derived cell lines did not correlate with infection efficacy and may not be a relevant indicator of clinical oncolytic potency. Adenovirus receptor analysis should be preferentially performed on biopsies obtained perioperatively.

Identifiers

PMID28797937
PMCPMC5610111
OpenAlexW2744535862

What OpenQuestion holds

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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.