Evidence map›Paper›PMID 22431921›Full record

ArticleNeoplasia (New York, N.Y.)2012

Efficacy of Tie2 receptor antagonism in angiosarcoma.

Jason R Hasenstein, Kelsey Kasmerchak, Darya Buehler, Gholam Reza Hafez, Kevin Cleary, John S Moody, Kevin R Kozak

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Targeting the Tie2-αBMC biology · 2018
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Generation of a murine hepatic angiosarcoma cell line and reproducible mouse tumor model.Laboratory investigation; a journal of technical methods and pathology · 2015
    Article
  18. Article
  19. Article
  20. Expression of angiopoietin-TIE system components in angiosarcoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2013
    Article
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.

Jason R HasensteinDepartment of Human Oncology, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Kelsey Kasmerchak
Darya Buehler
Gholam Reza Hafez
Kevin Cleary
John S Moody
Kevin R Kozak
University of Wisconsin–Madison · USRegional Cancer Center · US

Funding

INSTITUTIONAL CTSA (UW-MADISON): CLINICAL TRIALSUL1RR025011 · NCRR · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2007 to 2011
$29.5M
NCRR NIH HHS 1UL1RR25011NCRR NIH HHS UL1 RR025011
6 · The paper itself

Abstract

Angiosarcomas are malignant endothelial cell tumors with few effective systemic treatments. Despite a unique endothelial origin, molecular candidates for targeted therapeutic intervention have been elusive. In this study, we explored the tunica internal endothelial cell kinase 2 (Tie2) receptor as a potential therapeutic target in angiosarcoma. Human angiosarcomas from diverse sites were shown to be universally immunoreactive for Tie2. Tie2 and vascular endothelial growth factor receptor (VEGFR) antagonists inhibited SVR and MS1-VEGF angiosarcoma cell survival in vitro. In the high-grade SVR cell line, Tie2 and VEGF antagonists inhibited cell survival synergistically, whereas effects were largely additive in the low-grade MS1-VEGF cell line. Xenograft modeling using these cell lines closely recapitulated the human disease. In vivo, Tie2 and VEGFR inhibition resulted in significant angiosarcoma growth delay. The combination proved more effective than either agent alone. Tie2 inhibition seemed to elicit tumor growth delay through increased tumor cell apoptosis, whereas VEGFR inhibition reduced tumor growth by lowering tumor cell proliferation. These data identify Tie2 antagonism as a potential novel, targeted therapy for angiosarcomas and provide a foundation for further investigation of Tie2 inhibition, alone and in combinations, in the management of this disease.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisCell Line, TumorCell ProliferationCell SurvivalFemaleHemangiosarcomaHumansImidazolesIndolesMiceMice, NudePyridinesPyrrolesReceptors, Vascular Endothelial Growth Factor4-(6-methoxy-2-naphthyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imidazoleImidazolesIndolesPyridinesPyrrolesReceptors, Vascular Endothelial Growth FactorReceptor, TIE-2Sunitinib

Identifiers

PMID22431921
PMCPMC3306258
OpenAlexW1226199980

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.