Evidence map›Paper›PMID 23552414›Full record

ArticleJournal of virology2013

Vesicular stomatitis virus variants selectively infect and kill human melanomas but not normal melanocytes.

Guido Wollmann, John N Davis, Marcus W Bosenberg, Anthony N van den Pol

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Recent advancements in the diagnosis and treatment of acral melanoma.Journal of Zhejiang University. Science. B · 2024
    Review
  6. Review
  7. Oncolytic viruses in melanoma.Frontiers in bioscience (Landmark edition) · 2022
    Review
  8. Review
  9. Article
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  11. Article
  12. Review
  13. 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

4 authors at 1 institution in 1 country.

Guido WollmannDepartment of Neurosurgery, Yale University School of Medicine, New Haven, Connecticut, USA.
John N Davis
Marcus W Bosenberg
Anthony N van den Pol
Yale University · US

Funding

Yale SPORE in Skin CancerP50CA121974 · NCI · YALE UNIVERSITY · PI DAVID F STERN · 2006 to 2026
$43.9M
Vesicular stomatitis VSVrp30 selectively destroys human metastatic melanomaR01CA161048 · NCI · YALE UNIVERSITY · PI VAN DEN POL, ANTHONY N · 2012 to 2016
$1.7M
Oncolytic Virus Targets Brain TumorsR01CA124737 · NCI · YALE UNIVERSITY · PI VAN DEN POL, ANTHONY N · 2007 to 2011
$1.6M
The Role of Beta-catenin Signaling in Malignant MelanomaR01CA112054 · NCI · YALE UNIVERSITY · PI BOSENBERG, MARCUS W · 2005 to 2009
$1.4M
LuIII parvovirus targets gliomaR01CA175577 · NCI · YALE UNIVERSITY · PI VAN DEN POL, ANTHONY N · 2013 to 2015
$1.0M
NCI NIH HHS 1 P50 CA121974NCI NIH HHS CA112054NCI NIH HHS CA124737NCI NIH HHS CA161048NCI NIH HHS CA175577NCI NIH HHS P50 CA121974NCI NIH HHS R01 CA112054NCI NIH HHS R01 CA124737NCI NIH HHS R01 CA161048NCI NIH HHS R01 CA175577
6 · The paper itself

Abstract

Metastatic malignant melanoma remains one of the most therapeutically challenging forms of cancer. Here we test replication-competent vesicular stomatitis viruses (VSV) on 19 primary human melanoma samples and compare these infections with those of normal human melanocyte control cells. Even at a low viral concentration, we found a strong susceptibility to viral oncolysis in over 70% of melanomas. In contrast, melanocytes displayed strong resistance to virus infection and showed complete protection by interferon. Several recombinant VSVs were compared, and all infected and killed most melanomas with differences in the time course with increasing rates of melanoma infection, as follows: VSV-CT9-M51 < VSV-M51 < VSV-G/GFP < VSV-rp30. VSV-rp30 sequencing revealed 2 nonsynonymous mutations at codon positions P126 and L223, both of which appear to be required for the enhanced phenotype. VSV-rp30 showed effective targeting and infection of multiple subcutaneous and intracranial melanoma xenografts in SCID mice after tail vein virus application. Sequence analysis of mutations in the melanomas used revealed that BRAF but not NRAS gene mutation status was predictive for enhanced susceptibility to infection. In mouse melanoma models with specific induced gene mutations including mutations of the Braf, Pten, and Cdkn2a genes, viral infection correlated with the extent of malignant transformation. Similar to human melanocytes, mouse melanocytes resisted VSV-rp30 infection. This study confirms the general susceptibility of the majority of human melanoma types for VSV-mediated oncolysis.

Indexed as

AnimalsCell Line, TumorHumansMelanocytesMelanomaMiceMice, SCIDMutationOncolytic VirotherapyOncolytic VirusesProto-Oncogene Proteins B-rafTransplantation, HeterologousVesicular stomatitis Indiana virusVirus ReplicationXenograft Model Antitumor AssaysBRAF protein, humanProto-Oncogene Proteins B-raf

Identifiers

PMID23552414
PMCPMC3676084
OpenAlexW2132105061

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.