Evidence map›Paper›PMID 25071017›Full record

ArticleOncotarget2014

Eradication of metastatic melanoma through cooperative expression of RNA-based HDAC1 inhibitor and p73 by oncolytic adenovirus.

Holger Schipper, Vijay Alla, Claudia Meier, Dirk M Nettelbeck, Ottmar Herchenröder, Brigitte M Pützer

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Deacetylation of Transcription Factors in Carcinogenesis.International journal of molecular sciences · 2021
    Review
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  5. Article
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  7. Article
  8. Localized Treatment with Oncolytic Adenovirus Delta-24-RGDOX Induces Systemic Immunity against Disseminated Subcutaneous and Intracranial Melanomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
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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

6 authors at 2 institutions in 1 country.

Holger SchipperInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany; These authors contributed equally to the work.
Vijay AllaInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany; These authors contributed equally to the work.
Claudia MeierInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
Dirk M NettelbeckHelmholtz University Group Oncolytic Adenoviruses, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Ottmar HerchenröderInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
Brigitte M PützerInstitute of Experimental Gene Therapy and Cancer Research, Rostock University Medical Center, Rostock, Germany.
University of Rostock · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant melanoma is a highly aggressive cancer that retains functional p53 and p73, and drug unresponsiveness largely depends on defects in death pathways after epigenetic gene silencing in conjunction with an imbalanced p73/DNp73 ratio. We constructed oncolytic viruses armed with an inhibitor of deacetylation and/or p73 to specifically target metastatic cancer. Arming of the viruses is aimed at lifting epigenetic blockage and re-opening apoptotic programs in a staggered manner enabling both, efficient virus replication and balanced destruction of target cells through apoptosis. Our results showed that cooperative expression of shHDAC1 and p73 efficiently enhances apoptosis induction and autophagy of infected cells which reinforces progeny production. In vitro analyses revealed 100% cytotoxicity after infecting cells with OV.shHDAC1.p73 at a lower virus dose compared to control viruses. Intriguingly, OV.shHDAC1.p73 acts as a potent inhibitor of highly metastatic xenograft tumors in vivo. Tumor expansion was significantly reduced after intratumoral injection of 3 x 10⁸ PFU of either OV.shHDAC1 or OV.p73 and, most important, complete regression could be achieved in 100 % of tumors treated with OV.shHDAC1.p73. Our results point out that the combination of high replication capacity and simultaneous restoration of cell death routes significantly enhance antitumor activity.

Indexed as

AdenoviridaeCell Line, TumorDNA-Binding ProteinsGene Knockdown TechniquesHEK293 CellsHistone Deacetylase 1HumansMelanomaNuclear ProteinsOncolytic VirotherapyOncolytic VirusesRNA, Small InterferingTransgenesTumor Protein p73Tumor Suppressor ProteinsDNA-Binding ProteinsHDAC1 protein, humanHistone Deacetylase 1Nuclear ProteinsRNA, Small InterferingTP73 protein, humanTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID25071017
PMCPMC4171600
OpenAlexW1854850977

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.