Evidence map›Paper›PMID 34036669›Full record

ArticleCancer science2021

Triple-mutated oncolytic herpes virus for treating both fast- and slow-growing tumors.

Hiroshi Fukuhara, Yuta Takeshima, Tomoki Todo

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Oncolytic HSV and cancer drug interactions: Current clinical status and future directions.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
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  13. Extracellular Vesicles and Viruses: Two Intertwined Entities.International journal of molecular sciences · 2023
    Review
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  15. Article
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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

3 authors at 2 institutions in 2 countries.

Hiroshi FukuharaDepartment of Urology, Kyorin University School of Medicine, Tokyo, Japan.
Yuta TakeshimaDivision of Innovative Cancer Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Tomoki TodoDivision of Innovative Cancer Therapy, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0003-0523-8010
Institute for Advanced Medical Research · USKyorin University · JP

Funding

Japan Agency for Medical Research and Development JP15cm0106015h0005Japan Agency for Medical Research and Development JP20cm0106252h0002Japan Society for the Promotion of Science 08049157Japan Society for the Promotion of Science 09013291Ministry of Education, Culture, Sports, Science and Technology 09028017
6 · The paper itself

Abstract

Oncolytic virus therapy has emerged as a promising treatment option against cancer. To date, oncolytic viruses have been developed for malignant tumors, but the need for this new therapeutic modality also exists for benign and slow-growing tumors. G47∆ is an oncolytic herpes simplex virus type 1 (HSV-1) with an enhanced replication capability highly selective to tumor cells due to genetically engineered, triple mutations in the γ34.5, ICP6 and α47 genes. To create a powerful, but safe oncolytic HSV-1 that replicates efficiently in tumors regardless of growth speed, we used a bacterial artificial chromosome system that allows a desired promoter to regulate the expression of the ICP6 gene in the G47∆ backbone. Restoration of the ICP6 function in a tumor-specific manner using the hTERT promoter led to a highly capable oncolytic HSV-1. T-hTERT was more efficacious in the slow-growing OS-RC-2 and DU145 tumors than the control viruses, while retaining a high efficacy in the fast-growing U87MG tumors. The safety features are also retained, as T-hTERT proved safe when inoculated into the brain of HSV-1 sensitive A/J mice. This new technology should facilitate the use of oncolytic HSV-1 for all tumors irrespective of growth speed.

Indexed as

AnimalsBrain NeoplasmsCell Line, TumorChlorocebus aethiopsChromosomes, Artificial, BacterialFemaleGlioblastomaHerpesvirus 1, HumanHumansImmediate-Early ProteinsMiceMutationOncolytic VirotherapyOncolytic VirusesPromoter Regions, GeneticTelomerasegamma 34.5 protein, Human herpesvirus 1herpes simplex virus type 1-protein ICP6ICP47 protein, Herpes simplex virusImmediate-Early ProteinsTelomeraseTERT protein, humanViral ProteinsG47∆herpes simplex virus type 1hTERTICP6oncolytic virus

Identifiers

PMID34036669
PMCPMC8353919
OpenAlexW3165124657

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.