Evidence map›Paper›PMID 19521665›Full record

ArticleJournal of neuro-oncology2009

Engineered herpes simplex viruses efficiently infect and kill CD133+ human glioma xenograft cells that express CD111.

Gregory K Friedman, Catherine P Langford, Jennifer M Coleman, Kevin A Cassady, Jacqueline N Parker, James M Markert, G Yancey Gillespie

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuro-oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

61 citing papers in PubMed, 74 citations in OpenAlex.

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  18. Oncolytic Virotherapy in Glioma Tumors.International journal of molecular sciences · 2020
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1 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Gregory K FriedmanBrain Tumor Research Program, Department of Pediatrics, University of Alabama at Birmingham, 1046 Tinsley Harrison Tower, 1900 University Boulevard, Birmingham, AL, 35294-0006, USA. GFriedman@peds.uab.edu.
Catherine P LangfordDepartment of Surgery, Division of Neurosurgery, University of Alabama at Birmingham, Birmingham, AL, 35294-0006, USA.
Jennifer M ColemanDepartment of Surgery, Division of Neurosurgery, University of Alabama at Birmingham, Birmingham, AL, 35294-0006, USA.
Kevin A CassadyBrain Tumor Research Program, Department of Pediatrics, University of Alabama at Birmingham, 1046 Tinsley Harrison Tower, 1900 University Boulevard, Birmingham, AL, 35294-0006, USA.
Jacqueline N ParkerBrain Tumor Research Program, Department of Pediatrics, University of Alabama at Birmingham, 1046 Tinsley Harrison Tower, 1900 University Boulevard, Birmingham, AL, 35294-0006, USA.
James M MarkertBrain Tumor Research Program, Department of Pediatrics, University of Alabama at Birmingham, 1046 Tinsley Harrison Tower, 1900 University Boulevard, Birmingham, AL, 35294-0006, USA.
G Yancey GillespieDepartment of Surgery, Division of Neurosurgery, University of Alabama at Birmingham, Birmingham, AL, 35294-0006, USA.
University of Alabama at Birmingham · US

Funding

Virus Production CoreP01CA071933 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WEICHSELBAUM, RALPH R · 1997 to 2013
$14.5M
Viral and molecular chemotherapy of malignant CNS tumorsP50CA097247 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GILLESPIE, G. YANCEY · 2002 to 2009
$13.5M
NCI NIH HHS CA071933NCI NIH HHS CA097247NCI NIH HHS P01 CA071933NCI NIH HHS P50 CA097247
6 · The paper itself

Abstract

Oncolytic herpes simplex viruses (HSV) hold promise for therapy of glioblastoma multiforme (GBM) resistant to traditional therapies. We examined the ability of genetically engineered HSV to infect and kill cells that express CD133, a putative marker of glioma progenitor cells (GPC), to determine if GPC have an inherent therapeutic resistance to HSV. Expression of CD133 and CD111 (nectin-1), the major entry molecule for HSV, was variable in six human glioma xenografts, at initial disaggregation and after tissue culture. Importantly, both CD133+ and CD133- populations of glioma cells expressed CD111 in similar relative proportions in five xenografts, and CD133+ and CD133- glioma cell subpopulations were equally sensitive to killing in vitro by graded dilutions of wild-type HSV-1(F) or several different gamma(1)34.5-deleted viruses. GPC did not display an inherent resistance to HSV. While CD111 expression was an important factor for determining sensitivity of glioma cells to HSV oncolysis, it was not the only factor. Our findings support the notion that HSV will not be able to effectively enter, infect, and kill cells in tumors that have low CD111 expression (<20%). However, virotherapy with HSV may be very effective against CD111+ GPC resistant to traditional therapies.

Indexed as

Oncolytic VirotherapyAC133 AntigenAnimalsAntigens, CDBrain NeoplasmsCell Adhesion MoleculesCytopathogenic Effect, ViralGenetic EngineeringGenetic VectorsGlioblastomaGlycoproteinsHerpesvirus 1, HumanHumansMiceMice, NudeNectinsAC133 AntigenAntigens, CDCell Adhesion MoleculesGlycoproteinsNECTIN1 protein, humanNectin1 protein, mouseNectinsPeptidesPROM1 protein, humanProm1 protein, mouse

Identifiers

PMID19521665
PMCPMC4574288
OpenAlexW2071151466

What OpenQuestion holds

Textmetadata
LicenceTDM
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.