Evidence map›Paper›PMID 38400597›Full record

ArticleMolecular oncology2024

STING activator 2'3'-cGAMP enhanced HSV-1-based oncolytic viral therapy.

Patricia Angela Sibal, Shigeru Matsumura, Toru Ichinose, Itzel Bustos-Villalobos, Daishi Morimoto, Ibrahim R Eissa, Mohamed Abdelmoneim, Mona Alhussein Mostafa Aboalela, Nobuaki Mukoyama, Maki Tanaka and 2 more

Abstract read
In one paragraph

Article in Molecular oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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

12 authors.

Patricia Angela SibalCancer Immune Therapy Research Center, Graduate School of Medicine, Nagoya University, Japan.ORCID 0000-0002-0093-3519
Shigeru MatsumuraCancer Immune Therapy Research Center, Graduate School of Medicine, Nagoya University, Japan.
Toru IchinoseCancer Immune Therapy Research Center, Graduate School of Medicine, Nagoya University, Japan.
Itzel Bustos-VillalobosCancer Immune Therapy Research Center, Graduate School of Medicine, Nagoya University, Japan.
Daishi MorimotoDepartment of Surgery II, Graduate School of Medicine, Nagoya University, Japan.
Ibrahim R EissaCancer Immune Therapy Research Center, Graduate School of Medicine, Nagoya University, Japan.
Mohamed AbdelmoneimCancer Immune Therapy Research Center, Graduate School of Medicine, Nagoya University, Japan.
Mona Alhussein Mostafa AboalelaCancer Immune Therapy Research Center, Graduate School of Medicine, Nagoya University, Japan.
Nobuaki MukoyamaDepartment of Otolaryngology Graduate School of Medicine, Nagoya University, Japan.
Maki TanakaTakara Bio Inc., Kusatsu, Japan.
Yoshinori NaoeCancer Immune Therapy Research Center, Graduate School of Medicine, Nagoya University, Japan.
Hideki KasuyaCancer Immune Therapy Research Center, Graduate School of Medicine, Nagoya University, Japan.

Funding

Japan Grant-in-Aid for Scientific Research 16H05413Japan Grant-in-Aid for Scientific Research 16K15611Japan Grant-in-Aid for Scientific Research 18H02691Takara Bio, Inc
6 · The paper itself

Abstract

Oncolytic viruses (OVs) can selectively replicate in tumor cells and remodel the microenvironment of immunologically cold tumors, making them a promising strategy to evoke antitumor immunity. Similarly, agonists of the stimulator of interferon genes (STING)-interferon (IFN) pathway, the main cellular antiviral system, provide antitumor benefits by inducing the activation of dendritic cells (DC). Considering how the activation of the STING-IFN pathway could potentially inhibit OV replication, the use of STING agonists alongside OV therapy remains largely unexplored. Here, we explored the antitumor efficacy of combining an HSV-1-based OV, C-REV, with a membrane-impermeable STING agonist, 2'3'-GAMP. Our results demonstrated that tumor cells harbor a largely defective STING-IFN pathway, thereby preventing significant antiviral IFN induction regardless of the permeability of the STING agonist. In vivo, the combination therapy induced more proliferative KLRG1-high PD1-low CD8

Indexed as

Herpesvirus 1, HumanMembrane ProteinsNucleotides, CyclicOncolytic VirotherapyAnimalsCD8-Positive T-LymphocytesCell Line, TumorCombined Modality TherapyDendritic CellsFemaleHumansMiceMice, Inbred C3HMice, Inbred C57BLOncolytic VirusesSTING Proteincyclic guanosine monophosphate-adenosine monophosphateMembrane ProteinsNucleotides, CyclicSting1 protein, mouseSTING Protein2′3′‐cGAMPHSV1oncolytic viruspancreatic cancerSTING

Identifiers

PMID38400597
PMCPMC11076993

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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.