Evidence map›Paper›PMID 25231172›Full record

ArticleGene therapy2015

Clonal variation in interferon response determines the outcome of oncolytic virotherapy in mouse CT26 colon carcinoma model.

J J Ruotsalainen, M U Kaikkonen, M Niittykoski, M W Martikainen, C G Lemay, J Cox, N S De Silva, A Kus, T J Falls, J-S Diallo and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 35 citations in OpenAlex.

  1. VSVNature communications · 2024
    Article
  2. Article
  3. Review
  4. Personalizing Oncolytic Immunovirotherapy Approaches.Molecular diagnosis & therapy · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Multi-modal Potentiation of Oncolytic Virotherapy by Vanadium Compounds.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
    Article
  16. Article
  17. Article
  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

15 authors at 3 institutions in 2 countries.

J J RuotsalainenA.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, Kuopio, Finland.
M U KaikkonenA.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, Kuopio, Finland.
M NiittykoskiA.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, Kuopio, Finland.
M W MartikainenA.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, Kuopio, Finland.
C G LemayCentre for Innovative Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, Canada.
J CoxCentre for Innovative Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, Canada.
N S De SilvaCentre for Innovative Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, Canada.
A KusCentre for Innovative Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, Canada.
T J FallsCentre for Innovative Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, Canada.
J-S DialloCentre for Innovative Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, Canada.
F Le BoeufCentre for Innovative Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, Canada.
J C BellCentre for Innovative Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, Canada.
S Ylä-HerttualaA.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, Kuopio, Finland.
A E HinkkanenA.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, Kuopio, Finland.
M J Vähä-KoskelaCentre for Innovative Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, Canada.
Ottawa Hospital Research InstituteUniversity of Eastern Finland · FIOttawa Hospital · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

In our earlier studies, Semliki Forest virus vector VA7 completely eliminated type I interferon (IFN-I)-unresponsive human U87-luc glioma xenografts, whereas interferon-responsive mouse gliomas proved refractory. Here, we describe in two clones of CT26 murine colon carcinoma, opposed patterns of IFN-I responsiveness and sensitivity to VA7. Both CT26WT and CT26LacZ clones secreted biologically active interferon in vitro upon virus infection but only CT26WT cells were protected. Focal infection of CT26WT cultures was self-limiting but could be rescued using IFN-I pathway inhibitor Ruxolitinib or antibody against IFNβ. Whole transcriptome sequencing (RNA-Seq) and protein expression analysis revealed that CT26WT cells constitutively expressed 56 different genes associated with pattern recognition and IFN-I signaling pathways, spanning two reported anti-RNA virus gene signatures and 22 genes with reported anti-alphaviral activity. Whereas CT26WT tumors were strictly virus-resistant in vivo, infection of CT26LacZ tumors resulted in complete tumor eradication in both immunocompetent and severe combined immune deficient mice. In double-flank transplantation experiments, CT26WT tumors grew despite successful eradication of CT26LacZ tumors from the contralateral flank. Tumor growth progressed uninhibited also when CT26LacZ inoculums contained only a small fraction of CT26WT cells, demonstrating dominance of IFN responsiveness when heterogeneous tumors are targeted with interferon-sensitive oncolytic viruses.

Indexed as

Oncolytic VirotherapyAnimalsAntineoplastic AgentsBystander EffectCell Line, TumorColonic NeoplasmsGenetic VectorsGreen Fluorescent ProteinsInterferon-betaInterferon Type IMice, Inbred BALB CNecrosisNeoplasm TransplantationOncolytic VirusesSemliki forest virusSTAT1 Transcription FactorAntineoplastic Agentsenhanced green fluorescent proteinGreen Fluorescent ProteinsInterferon-betaInterferon Type IStat1 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID25231172
OpenAlexW2010328268

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.