Evidence map›Paper›PMID 32597867›Full record

ArticleJournal of visualized experiments : JoVE2020

A Patient-Derived Xenograft Model for Venous Malformation.

Sandra Schrenk, Jillian Goines, Elisa Boscolo

Open access · greenAbstract readVideo-Audio Media
In one paragraph

Article in Journal of visualized experiments : JoVE, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Semaphorin 3A and 3F Promote Lumen Expansion in TIE2-Mutated Venous Malformation.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
  6. Article
  7. Article
  8. 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

3 authors at 1 institution in 1 country.

Sandra Schrenk *Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center.
Jillian Goines *Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center.
Elisa BoscoloDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center; Department of Pediatrics, University of Cincinnati College of Medicine; Elisa.Boscolo@cchmc.org.
Cincinnati Children's Hospital Medical Center · US

Funding

Venous Malformations (VM): A Murine Model to Identify Therapies to Target AberranR01HL117952 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI BOSCOLO, ELISA · 2013 to 2025
$4.9M
NHLBI NIH HHS R01 HL117952
6 · The paper itself

Abstract

Venous malformation (VM) is a vascular anomaly that arises from impaired development of the venous network resulting in dilated and often dysfunctional veins. The purpose of this article is to carefully describe the establishment of a murine xenograft model that mimics human VM and is able to reflect patient heterogeneity. Hyper-activating non-inherited (somatic) TEK (TIE2) and PIK3CA mutations in endothelial cells (EC) have been identified as the main drivers of pathological vessel enlargement in VM. The following protocol describes the isolation, purification and expansion of patient-derived EC expressing mutant TIE2 and/or PIK3CA. These EC are injected subcutaneously into the back of immunodeficient athymic mice to generate ectatic vascular channels. Lesions generated with TIE2 or PIK3CA-mutant EC are visibly vascularized within 7‒9 days of injection and recapitulate histopathological features of VM patient tissue. This VM xenograft model provides a reliable platform to investigate the cellular and molecular mechanisms driving VM formation and expansion. In addition, this model will be instrumental for translational studies testing the efficacy of novel drug candidates in preventing the abnormal vessel enlargement seen in human VM.

Indexed as

HeterograftsAnimalsCell ProliferationClass I Phosphatidylinositol 3-KinasesCollagenasesDisease Models, AnimalEndothelial CellsFibronectinsHumansInjections, SubcutaneousMaleMice, NudeSclerotherapyVascular MalformationsVeinsClass I Phosphatidylinositol 3-KinasesCollagenasesFibronectinsPIK3CA protein, human

Identifiers

PMID32597867
PMCPMC7457366
OpenAlexW3036633649

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.