Evidence map›Paper›PMID 20473328›Full record

ArticleOncogene2010

The viral tropism of two distinct oncolytic viruses, reovirus and myxoma virus, is modulated by cellular tumor suppressor gene status.

M Kim, C T Williamson, J Prudhomme, D G Bebb, K Riabowol, P W K Lee, S P Lees-Miller, Y Mori, M M Rahman, G McFadden and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Optimal delivery of RNA interference by viral vectors for cancer therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Oncolytic Virotherapy with Myxoma Virus.Journal of clinical medicine · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

11 authors at 3 institutions in 2 countries.

M KimDepartment of Biochemistry and Molecular Biology, University of Calgary, Calgary, Alberta, Canada.
C T Williamson
J Prudhomme
D G Bebb
K Riabowol
P W K Lee
S P Lees-Miller
Y Mori
M M Rahman
G McFadden
R N Johnston
University of Calgary · CAUniversity of Florida · USDalhousie University · CA

Funding

Studies in Poxvirus Host Range Genes and TropismR01AI080607 · NIAID · UNIVERSITY OF FLORIDA · PI RAHMAN, MASMUDUR MOHAMMED · 2009 to 2025
$5.6M
Myxoma Virus (MV) Oncolysis for treating human cancerR01CA138541 · NCI · UNIVERSITY OF FLORIDA · PI MCFADDEN, GRANT · 2010 to 2014
$1.5M
CIHRHoward Hughes Medical InstituteNCI NIH HHS R01 CA138541NIAID NIH HHS R01 AI080607
6 · The paper itself

Abstract

Replication-competent oncolytic viruses hold great potential for the clinical treatment of many cancers. Importantly, many oncolytic virus candidates, such as reovirus and myxoma virus, preferentially infect cancer cells bearing abnormal cellular signaling pathways. Reovirus and myxoma virus are highly responsive to activated Ras and Akt signaling pathways, respectively, for their specificity for viral oncolysis. However, considering the complexity of cancer cell populations, it is possible that other tumor-specific signaling pathways may also contribute to viral discrimination between normal versus cancer cells. Because carcinogenesis is a multistep process involving the accumulation of both oncogene activations and the inactivation of tumor suppressor genes, we speculated that not only oncogenes but also tumor suppressor genes may have an important role in determining the tropism of these viruses for cancer cells. It has been previously shown that many cellular tumor suppressor genes, such as p53, ATM and Rb, are important for maintaining genomic stability; dysfunction of these tumor suppressors may disrupt intact cellular antiviral activity due to the accumulation of genomic instability or due to interference with apoptotic signaling. Therefore, we speculated that cells with dysfunctional tumor suppressors may display enhanced susceptibility to challenge with these oncolytic viruses, as previously seen with adenovirus. We report here that both reovirus and myxoma virus preferentially infect cancer cells bearing dysfunctional or deleted p53, ATM and Rb tumor suppressor genes compared to cells retaining normal counterparts of these genes. Thus, oncolysis by these viruses may be influenced by both oncogenic activation and tumor suppressor status.

Indexed as

Genes, Tumor SuppressorViral TropismAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell Line, TumorDNA-Binding ProteinsGene DeletionGene Knockdown TechniquesHumansMiceMyxoma virusNeoplasmsOncolytic VirusesProtein Serine-Threonine KinasesAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID20473328
PMCPMC4374435
OpenAlexW2078069375

What OpenQuestion holds

Textmetadata
LicenceTDM
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.