Evidence map›Paper›PMID 27022280›Full record

ArticleOncoTargets and therapy2016

Combination of vatalanib and a 20-HETE synthesis inhibitor results in decreased tumor growth in an animal model of human glioma.

Adarsh Shankar, Thaiz F Borin, Asm Iskander, Nadimpalli Rs Varma, Bhagelu R Achyut, Meenu Jain, Tom Mikkelsen, Austin M Guo, Wilson B Chwang, James R Ewing and 2 more

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  8. GPR75 receptor mediates 20-HETE-signaling and metastatic features of androgen-insensitive prostate cancer cells.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020
    Article
  9. 20-HETE synthesis inhibition promotes cerebral protection after intracerebral hemorrhage without inhibiting angiogenesis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    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

12 authors at 5 institutions in 2 countries.

Adarsh ShankarTumor Angiogenesis Laboratory, Cancer Center, Georgia Regents University, Augusta, GA, USA.
Thaiz F BorinLaboratory of Molecular Investigation of Cancer (LIMC), Faculty of Medicine of Sao Jose do Rio Preto, Sao Jose do Rio Preto, Brazil.
Asm IskanderTumor Angiogenesis Laboratory, Cancer Center, Georgia Regents University, Augusta, GA, USA.
Nadimpalli Rs VarmaDepartment of Radiology, Cellular and Molecular Imaging Laboratory, Detroit, MI, USA.
Bhagelu R AchyutTumor Angiogenesis Laboratory, Cancer Center, Georgia Regents University, Augusta, GA, USA.
Meenu JainTumor Angiogenesis Laboratory, Cancer Center, Georgia Regents University, Augusta, GA, USA.
Tom MikkelsenDepartment of Neurosurgery, Henry Ford Health System, Detroit, MI, USA.
Austin M GuoDepartment of Pharmacology, New York Medical College, Valhalla, NY, USA.
Wilson B ChwangDepartment of Radiology, Cellular and Molecular Imaging Laboratory, Detroit, MI, USA.
James R EwingDepartment of Neurology and Radiology, Henry Ford Health System, Detroit, MI, USA.
Hassan Bagher-EbadianDepartment of Neurology and Radiology, Henry Ford Health System, Detroit, MI, USA.
Ali S ArbabTumor Angiogenesis Laboratory, Cancer Center, Georgia Regents University, Augusta, GA, USA.
Georgia Regents Medical Center · USHenry Ford Health System · USAugusta University · USFaculdade de Medicina de São José do Rio Preto · BRNew York Medical College · US

Funding

Understanding Mechanisms of Resistance to Anti-angiogenic TreatmentsR01CA160216 · NCI · HENRY FORD HEALTH SYSTEM · PI ARBAB, ALI SYED · 2012 to 2016
$1.8M
In vivo detection of involvement of endogenous BM progenitor cells in gliomaR01CA172048 · NCI · HENRY FORD HEALTH SYSTEM · PI ARBAB, ALI SYED · 2012 to 2014
$894k
NCI NIH HHS R01 CA160216NCI NIH HHS R01 CA172048
6 · The paper itself

Abstract

backgroundDue to the hypervascular nature of glioblastoma (GBM), antiangiogenic treatments, such as vatalanib, have been added as an adjuvant to control angiogenesis and tumor growth. However, evidence of progressive tumor growth and resistance to antiangiogenic treatment has been observed. To counter the unwanted effect of vatalanib on GBM growth, we have added a new agent known as N-hydroxy-N'-(4-butyl-2 methylphenyl)formamidine (HET0016), which is a selective inhibitor of 20-hydroxyeicosatetraenoic acid (20-HETE) synthesis. The aims of the studies were to determine 1) whether the addition of HET0016 can attenuate the unwanted effect of vatalanib on tumor growth and 2) whether the treatment schedule would have a crucial impact on controlling GBM.

methodsU251 human glioma cells (4×10(5)) were implanted orthotopically. Two different treatment schedules were investigated. Treatment starting on day 8 (8-21 days treatment) of the tumor implantation was to mimic treatment following detection of tumor, where tumor would have hypoxic microenvironment and well-developed neovascularization. Drug treatment starting on the same day of tumor implantation (0-21 days treatment) was to mimic cases following radiation therapy or surgery. There were four different treatment groups: vehicle, vatalanib (oral treatment 50 mg/kg/d), HET0016 (intraperitoneal treatment 10 mg/kg/d), and combined (vatalanib and HET0016). Following scheduled treatments, all animals underwent magnetic resonance imaging on day 22, followed by euthanasia. Brain specimens were equally divided for immunohistochemistry and protein array analysis.

resultsOur results demonstrated a trend that HET0016, alone or in combination with vatalanib, is capable of controlling the tumor growth compared with that of vatalanib alone, indicating attenuation of the unwanted effect of vatalanib. When both vatalanib and HET0016 were administered together on the day of the tumor implantation (0-21 days treatment), tumor volume, tumor blood volume, permeability, extravascular and extracellular space volume, tumor cell proliferation, and cell migration were decreased compared with that of the vehicle-treated group.

conclusionHET0016 is capable of controlling tumor growth and migration, but these effects are dependent on the timing of drug administration. The addition of HET0016 to vatalanib may attenuate the unwanted effect of vatalanib.

Indexed as

antiangiogenic treatmentsglioblastomaHET0016magnetic resonance imagingprotein arrayvascular parameters

Identifiers

PMID27022280
PMCPMC4790509
OpenAlexW2293241826

What OpenQuestion holds

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Registered trials

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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.