Evidence map›Paper›PMID 30101187›Full record

ArticleMolecular therapy oncolytics2018

Combination of IAP Antagonists and TNF-α-Armed Oncolytic Viruses Induce Tumor Vascular Shutdown and Tumor Regression.

Shawn T Beug, Stephanie J Pichette, Martine St-Jean, Janelle Holbrook, Danielle E Walker, Eric C LaCasse, Robert G Korneluk

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy oncolytics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Oncolytic Virotherapy in Solid Tumors: A Current Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. cIAP1/2 Antagonism Induces Antigen-Specific T Cell-Dependent Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
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  16. Review
  17. Article
  18. Article
  19. Review
  20. New Therapeutic Options for Advanced Hepatocellular Carcinoma.Cancer control : journal of the Moffitt Cancer Center
    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

7 authors at 2 institutions in 1 country.

Shawn T BeugApoptosis Research Center, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON, Canada.
Stephanie J PichetteApoptosis Research Center, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON, Canada.
Martine St-JeanApoptosis Research Center, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON, Canada.
Janelle HolbrookApoptosis Research Center, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON, Canada.
Danielle E WalkerApoptosis Research Center, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON, Canada.
Eric C LaCasseApoptosis Research Center, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON, Canada.
Robert G KornelukApoptosis Research Center, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON, Canada.
Children's Hospital of Eastern Ontario · CAUniversity of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Smac mimetic compounds (SMCs) are anti-cancer drugs that antagonize Inhibitor of Apoptosis proteins, which consequently sensitize cancer cells to death in the presence of proinflammatory ligands such as tumor necrosis factor alpha (TNF-α). SMCs synergize with the attenuated oncolytic vesicular stomatitis virus (VSVΔ51) by eliciting an innate immune response, which is dependent on the endogenous production of TNF-α and type I interferon. To improve on this SMC-mediated synergistic response, we generated TNF-α-armed VSVΔ51 to produce elevated levels of this death ligand. Due to ectopic expression of TNF-α from infected cells, a lower viral dose of TNF-α-armed VSVΔ51 combined with treatment of the SMC LCL161 was sufficient to improve the survival rate compared to LCL161 and unarmed VSVΔ51 co-therapy. This improved response is attributed to a bystander effect whereby the spread of TNF-α from infected cells leads to the death of uninfected cells in the presence of LCL161. In addition, the treatments induced vascular collapse in solid tumors with a concomitant increase of tumor cell death, revealing another mechanism by which cytokine-armed VSVΔ51 in combination with LCL161 can kill tumor cells. Our studies demonstrate the potential for cytokine-engineered oncolytic virus and SMCs as a new combination immunotherapy for cancer treatment.

Indexed as

cancercellular inhibitor of apoptosis 1/2cIAP1/cIAP2immunotherapyoncolytic virusSmac mimetic compoundSmac mimeticsSMCTNF-αtumor necrosis factor alphavascular collapsevesicular stomatitis virusVSV

Identifiers

PMID30101187
PMCPMC6076221
OpenAlexW2809465143

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.