Evidence map›Paper›PMID 32170083›Full record

ArticleNature communications2020

An engineered oncolytic virus expressing PD-L1 inhibitors activates tumor neoantigen-specific T cell responses.

Guan Wang, Xi Kang, Katherine S Chen, Tiffany Jehng, Lindsey Jones, Jie Chen, Xue F Huang, Si-Yi Chen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers.

0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

150 citing papers in PubMed, 214 citations in OpenAlex.

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  13. Immunotherapy: the Mega Weapon to Cure Cancer.Journal of family & reproductive health · 2026
    Review
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90 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

8 authors at 3 institutions in 2 countries.

Guan WangDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, 90033, CA, USA.
Xi KangDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, 90033, CA, USA.
Katherine S ChenFu Foundation School of Engineering and Applied Science, Columbia University, New York, 10023, NY, USA.
Tiffany JehngDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, 90033, CA, USA.
Lindsey JonesDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, 90033, CA, USA.
Jie ChenPomona Biotechnology Corp., Beijing, 100176, China.
Xue F Huang *Pomona Biotechnology Corp., Beijing, 100176, China. xuehuang2016@gmail.com.ORCID http://orcid.org/0000-0002-1957-7649
Si-Yi Chen *Department of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, 90033, CA, USA. siyichen@usc.edu.ORCID http://orcid.org/0000-0003-2403-4988
University of Southern California · USBeijing VDJBio (China) · CNColumbia University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncolytic viruses offer an in situ vaccination approach to activate tumor-specific T cell responses. However, the upregulation of PD-L1 expression on tumor cells and immune cells leads to tumor resistance to oncolytic immunotherapy. In this study, we generate an engineered oncolytic virus that coexpresses a PD-L1 inhibitor and GM-CSF. We find that the oncolytic virus is able to secrete the PD-L1 inhibitor that systemically binds and inhibits PD-L1 on tumor cells and immune cells. Importantly, the intratumoral injection with the oncolytic virus overcomes PD-L1-mediated immunosuppression during both the priming and effector phases, provokes systemic T cell responses against dominant and subdominant neoantigen epitopes derived from mutations, and leads to an effective rejection of both virus-injected and distant tumors. In summary, this engineered oncolytic virus is able to activate tumor neoantigen-specific T cell responses, providing a potent, individual tumor-specific oncolytic immunotherapy for cancer patients, especially those resistant to PD-1/PD-L1 blockade therapy.

Indexed as

Oncolytic VirotherapyAnimalsAntigens, NeoplasmAntineoplastic AgentsB7-H1 AntigenCD8-Positive T-LymphocytesCell Line, TumorDisease Models, AnimalGenetic EngineeringGranulocyte-Macrophage Colony-Stimulating FactorHEK293 CellsHumansImmunosuppression TherapyImmunotherapyMiceMice, Inbred C57BLAntigens, NeoplasmAntineoplastic AgentsB7-H1 AntigenCD274 protein, humanGranulocyte-Macrophage Colony-Stimulating FactorRecombinant Proteinssargramostim

Identifiers

PMID32170083
PMCPMC7070065
OpenAlexW3012532724

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.