Evidence map›Paper›PMID 25761895›Full record

ArticleMolecular cancer therapeutics2015

Enhancement of the proapoptotic properties of newcastle disease virus promotes tumor remission in syngeneic murine cancer models.

Sara Cuadrado-Castano, Juan Ayllon, Mena Mansour, Janis de la Iglesia-Vicente, Stefan Jordan, Shashank Tripathi, Adolfo García-Sastre, Enrique Villar

Abstract read
In one paragraph

Article in Molecular cancer therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
  2. Oncolytic viruses: advanced strategies in cancer therapy.Signal transduction and targeted therapy · 2026
    Review
  3. Article
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  6. Article
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  13. Article
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  15. Review
  16. Article
  17. Article
  18. Review
  19. Reverse Genetics of Newcastle Disease Virus.Methods in molecular biology (Clifton, N.J.) · 2017
    Article
  20. Review
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.

Sara Cuadrado-CastanoDepartment of Biochemistry and Molecular Biology, University of Salamanca, Salamanca, Spain. Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York.
Juan AyllonDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York. Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, New York.
Mena MansourDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York.
Janis de la Iglesia-VicenteDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York.
Stefan JordanDepartment of Oncological Sciences, Immunology Institute and the Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York.
Shashank TripathiDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York.
Adolfo García-SastreDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York. Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, New York. Division of Infectious Disease, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York. Adolfo.Garcia-Sastre@mssm.edu.
Enrique VillarDepartment of Biochemistry and Molecular Biology, University of Salamanca, Salamanca, Spain.

Funding

TRAINING PROGRAM IN CANCER THERAPYT32CA078207 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI James J Manfredi · 1999 to 2026
$11.6M
SUPPLEMENT TO: A Novel approach to RSV vaccinationR01AI088770 · NIAID · RBHS-NEW JERSEY MEDICAL SCHOOL · PI DURBIN, JOAN E. · 2010 to 2015
$3.7M
NCI NIH HHS T32 CA078207NIAID NIH HHS R01 AI088770NIAID NIH HHS R01AI088770
6 · The paper itself

Abstract

Newcastle disease virus (NDV) is considered a promising agent for cancer therapy due to its oncolytic properties. These include preferential replication in transformed cells, induction of innate and adaptive immune responses within tumors, and cytopathic effects in infected tumor cells due to the activation of apoptosis. To enhance the latter and thus possibly enhance the overall oncolytic activity of NDV, we generated a recombinant NDV encoding the human TNF receptor Fas (rNDV-B1/Fas). rNDV-B1/Fas replicates to similar titers as its wild-type (rNDV-B1) counterpart; however, overexpression of Fas in infected cells leads to higher levels of cytotoxicity correlated with faster and increased apoptosis responses, in which both the intrinsic and extrinsic pathways are activated earlier. Furthermore, in vivo studies in syngeneic murine melanoma models show an enhancement of the oncolytic properties of rNDV-B1/Fas, with major improvements in survival and tumor remission. Altogether, our data suggest that upregulation of the proapoptotic function of NDV is a viable approach to enhance its antitumor properties and adds to the currently known, rationally based strategies to design optimized therapeutic viral vectors for the treatment of cancer.

Indexed as

AnimalsApoptosisCell Line, TumorChlorocebus aethiopsfas ReceptorFemaleHeLa CellsHumansMelanoma, ExperimentalMiceNewcastle disease virusNIH 3T3 CellsOncolytic VirotherapyOncolytic VirusesSkin NeoplasmsVero CellsFAS protein, humanfas Receptor

Identifiers

PMID25761895
PMCPMC4425597

What OpenQuestion holds

Textmetadata
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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.