Evidence map›Paper›PMID 16840332›Full record

ArticleJournal of virology2006

Newcastle disease virus exerts oncolysis by both intrinsic and extrinsic caspase-dependent pathways of cell death.

Subbiah Elankumaran, Daniel Rockemann, Siba K Samal

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

122 citing papers in PubMed, 233 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Oncolytic Virotherapy in Solid Tumors: A Current Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. [Programmed cell death in paramyxovirus infection].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    Review
  9. Article
  10. Article
  11. Current status and research progress of oncolytic virus.Pharmaceutical science advances · 2024
    Review
  12. Article
  13. Article
  14. Review
  15. Molecular Circuits of Immune Sensing and Response to Oncolytic Virotherapy.International journal of molecular sciences · 2024
    Review
  16. Synergistic effects ofIranian journal of microbiology · 2024
    Article
  17. Oncolytic Virotherapy: A New Paradigm in Cancer Immunotherapy.International journal of molecular sciences · 2024
    Review
  18. Article
  19. Article
  20. Article

62 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

3 authors at 1 institution in 1 country.

Subbiah ElankumaranVirginia-Maryland Regional College of Veterinary Medicine, University of Maryland, College Park, MD 20742, USA.
Daniel Rockemann
Siba K Samal
University of Maryland, College Park · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Newcastle disease virus (NDV), an avian paramyxovirus, is tumor selective and intrinsically oncolytic. Here, we present evidence that genetically modified, recombinant NDV strains are cytotoxic to human tumor cell lines of ecto-, endo-, and mesodermal origin. We show that cytotoxicity against tumor cells is due to multiple caspase-dependent pathways of apoptosis independent of interferon signaling competence. The signaling pathways of NDV-induced, cancer cell-selective apoptosis are not well understood. We demonstrate that NDV triggers apoptosis by activating the mitochondrial/intrinsic pathway and that it acts independently of the death receptor/extrinsic pathway. Caspase-8-methylated SH-SY5Y neuroblastoma cells are as sensitive to NDV as other caspase-8-competent cells. This demonstrates that NDV is likely to act primarily through the mitochondrial death pathway. NDV infection results in the loss of mitochondrial membrane potential and the subsequent release of the mitochondrial protein cytochrome c, but the second mitochondrion-derived activator of caspase (Smac/DIABLO) is not released. In addition, we describe early activation of caspase-9 and caspase-3. In contrast, cleavage of caspase-8, which is predominantly activated by the death receptor pathway, is a TNF-related, apoptosis-inducing ligand (TRAIL)-induced late event in NDV-mediated apoptosis of tumor cells. Our data, therefore, indicate that the death signal(s) generated by NDV in tumor cells ultimately converges at the mitochondria and that it acts independently of the death receptor pathway. Our cytotoxicity studies demonstrate that recombinant NDV could be developed as a cancer virotherapy agent, either alone or in combination with therapeutic transgenes. We have also shown that trackable oncolytic NDV could be developed without any reduction in oncolytic efficacy.

Indexed as

ApoptosisAnimalsApoptosis Regulatory ProteinsBlotting, WesternCarcinoma, HepatocellularCaspasesChick EmbryoChickensCytochromes cFibroblastsHeLa CellsHumansIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsMembrane PotentialsMitochondriaApoptosis Regulatory ProteinsCaspasesCytochromes cDIABLO protein, humanIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsMitochondrial ProteinsTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID16840332
PMCPMC1563725
OpenAlexW2099295163

What OpenQuestion holds

Textmetadata
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.