Evidence map›Paper›PMID 32088771›Full record

ArticleCancer immunology, immunotherapy : CII2020

Oncolytic Newcastle disease virus activation of the innate immune response and priming of antitumor adaptive responses in vitro.

Shannon Burke, Amy Shergold, Matthew J Elder, Justine Whitworth, Xing Cheng, Hong Jin, Robert W Wilkinson, James Harper, Danielle K Carroll

Open access · hybridAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Oncolytic virotherapy and tumor microenvironment modulation.Clinical and experimental medicine · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article
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

9 authors at 3 institutions in 3 countries.

Shannon BurkeOncology R&D, AstraZeneca, Aaron Klug Building, Granta Park, Cambridge, CB21 6GH, UK. shannon.burke@astrazeneca.com.ORCID http://orcid.org/0000-0002-2876-7946
Amy ShergoldOncology R&D, AstraZeneca, Aaron Klug Building, Granta Park, Cambridge, CB21 6GH, UK.
Matthew J ElderOncology R&D, AstraZeneca, Aaron Klug Building, Granta Park, Cambridge, CB21 6GH, UK.
Justine WhitworthOncology R&D, AstraZeneca, Aaron Klug Building, Granta Park, Cambridge, CB21 6GH, UK.
Xing ChengBioPharmaceuticals R&D, Clinical Pharmacology & Safety Sciences, AstraZeneca, South San Francisco, CA, USA.
Hong JinBioPharmaceuticals R&D, Clinical Pharmacology & Safety Sciences, AstraZeneca, South San Francisco, CA, USA.
Robert W WilkinsonOncology R&D, AstraZeneca, Aaron Klug Building, Granta Park, Cambridge, CB21 6GH, UK.
James HarperOncology R&D, AstraZeneca, Aaron Klug Building, Granta Park, Cambridge, CB21 6GH, UK.
Danielle K CarrollOncology R&D, AstraZeneca, Aaron Klug Building, Granta Park, Cambridge, CB21 6GH, UK.
AstraZeneca (United Kingdom) · GBNGM Biopharmaceuticals (United States) · USPocketLab (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncolytic virus (OV) therapy is an emerging approach with the potential to redefine treatment options across a range of cancer indications and in patients who remain resistant to existing standards of care, including immuno-oncology (IO) drugs. MEDI5395, a recombinant Newcastle disease virus (NDV), engineered to express granulocyte-macrophage colony-stimulating factor (GM-CSF), exhibits potent oncolytic activity. It was hypothesized that activation of immune cells by MEDI5395, coupled with its oncolytic activity, would enhance the priming of antitumor immunity. Using MEDI5395 and recombinant NDVs encoding fluorescent reporter genes, we demonstrated preferential virus uptake and non-productive infection in myeloid cells, including monocytes, macrophages, and dendritic cells (DCs). Infection resulted in immune-cell activation, with upregulation of cell surface activation markers (e.g., CD80, PD-L1, HLA-DR) and secretion of proinflammatory cytokines (IFN-α2a, IL-6, IL-8, TNF-α). Interestingly, in vitro M2-polarized macrophages were more permissive to virus infection than were M1-polarized macrophages. In a co-culture system, infected myeloid cells were effective virus vectors and mediated the transfer of infectious NDV particles to tumor cells, resulting in cell death. Furthermore, NDV-infected DCs stimulated greater proliferation of allogeneic T cells than uninfected DCs. Antigens released after NDV-induced tumor cell lysis were cross-presented by DCs and drove activation of tumor antigen-specific autologous T cells. MEDI5395 therefore exhibited potent immunostimulatory activity and an ability to enhance antigen-specific T-cell priming. This, coupled with its tumor-selective oncolytic capacity, underscores the promise of MEDI5395 as a multimodal therapeutic, with potential to both enhance current responding patient populations and elicit de novo responses in resistant patients.

Indexed as

Cell Line, TumorGenetic VectorsHumansImmunity, InnateNewcastle disease virusOncolytic VirotherapyOncolytic VirusesImmunotherapyMEDI5395Newcastle disease virusOncolytic virus

Identifiers

PMID32088771
PMCPMC7230062
OpenAlexW3007966471

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.