Evidence map›Paper›PMID 32210430›Full record

ArticlePloS one2020

Molecular subtypes in canine hemangiosarcoma reveal similarities with human angiosarcoma.

Guannan Wang, Ming Wu, Amy C Durham, Enrico Radaelli, Nicola J Mason, XiaoWei Xu, David B Roth

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.2field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  9. Article
  10. Review
  11. Review of Molecular Technologies for Investigating Canine Cancer.Animals : an open access journal from MDPI · 2024
    Review
  12. Parthenolide As a Therapeutic for Disseminated Canine Neoplasms.The Journal of pharmacology and experimental therapeutics · 2024
    Article
  13. Article
  14. Review
  15. Review
  16. 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

7 authors at 2 institutions in 1 country.

Guannan WangDepartment of Pathology and Laboratory Medicine, Raymond and Ruth Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.ORCID 0000-0003-0130-3241
Ming WuIllumina, San Diego, CA, United States of America.
Amy C DurhamDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.
Enrico RadaelliDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.ORCID 0000-0002-2885-0221
Nicola J MasonDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.
XiaoWei XuDepartment of Pathology and Laboratory Medicine, Raymond and Ruth Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.
David B RothDepartment of Pathology and Laboratory Medicine, Raymond and Ruth Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.
University of Pennsylvania · USIllumina (United States) · US

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Robert H. Vonderheide · 1985 to 2026
$222.3M
NCI NIH HHS P30 CA016520
6 · The paper itself

Abstract

Angiosarcoma (AS) is a rare neoplasm with limited treatment options and a poor survival rate. Development of effective therapies is hindered by the rarity of this disease. Dogs spontaneously develop hemangiosarcoma (HSA), a common, histologically similar neoplasm. Metastatic disease occurs rapidly and despite chemotherapy, most dogs die several months after diagnosis. These features suggest that HSA might provide a tractable model to test experimental therapies in clinical trials. We previously reported whole exome sequencing of 20 HSA cases. Here we report development of a NGS targeted resequencing panel to detect driver mutations in HSA and other canine tumors. We validated the panel by resequencing the original 20 cases and sequenced 30 additional cases. Overall, we identified potential driver mutations in over 90% of the cases, including well-documented (in human cancers) oncogenic mutations in PIK3CA (46%), PTEN (6%), PLCG1(4%), and TP53 (66%), as well as previously undetected recurrent activating mutations in NRAS (24%). The driver role of these mutations is further demonstrated by augmented downstream signaling crucial to tumor growth. The recurrent, mutually exclusive mutation patterns suggest distinct molecular subtypes of HSA. Driver mutations in some subtypes closely resemble those seen in some AS cases, including NRAS, PLCG1, PIK3CA and TP53. Furthermore, activation of the MAPK and PI3K pathways appear to be key oncogenic mechanisms in both species. Together, these observations suggest that dogs with spontaneous HSA could serve as a useful model for testing the efficacy of targeted therapies, some of which could potentially be of therapeutic value in AS.

Indexed as

AnimalsDog DiseasesDogsExomeExome SequencingGenes, NeoplasmHemangiosarcomaHumansMutationPhosphatidylinositol 3-Kinasesras ProteinsReproducibility of ResultsSignal TransductionPhosphatidylinositol 3-Kinasesras Proteins

Identifiers

PMID32210430
PMCPMC7094861
OpenAlexW3014009429

What OpenQuestion holds

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LicenceCC BY
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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.