Evidence map›Paper›PMID 27429653›Full record

ArticleInternational journal of cancer research

Targeting Bone Marrow to Potentiate the Anti-Tumor Effect of Tyrosine Kinase Inhibitor in Preclinical Rat Model of Human Glioblastoma.

S Shaaban, M Alsulami, S A Arbab, R Ara, A Shankar, A Iskander, K Angara, M Jain, H Bagher-Ebadian, B R Achyut and 1 more

Open access · diamondAbstract read
In one paragraph

Article in International journal of cancer research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  3. Article
  4. Tumor angiogenesis: causes, consequences, challenges and opportunities.Cellular and molecular life sciences : CMLS · 2020
    Review
  5. Article
  6. 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

11 authors at 2 institutions in 1 country.

S ShaabanLaboratory of Tumor Angiogenesis, Department of Biochemistry and Molecular Biology, Cancer Center, Georgia Regents University, Augusta, GA, 30912, USA.
M AlsulamiLaboratory of Tumor Angiogenesis, Department of Biochemistry and Molecular Biology, Cancer Center, Georgia Regents University, Augusta, GA, 30912, USA.
S A ArbabLaboratory of Tumor Angiogenesis, Department of Biochemistry and Molecular Biology, Cancer Center, Georgia Regents University, Augusta, GA, 30912, USA.
R AraLaboratory of Tumor Angiogenesis, Department of Biochemistry and Molecular Biology, Cancer Center, Georgia Regents University, Augusta, GA, 30912, USA.
A ShankarLaboratory of Tumor Angiogenesis, Department of Biochemistry and Molecular Biology, Cancer Center, Georgia Regents University, Augusta, GA, 30912, USA.
A IskanderLaboratory of Tumor Angiogenesis, Department of Biochemistry and Molecular Biology, Cancer Center, Georgia Regents University, Augusta, GA, 30912, USA.
K AngaraLaboratory of Tumor Angiogenesis, Department of Biochemistry and Molecular Biology, Cancer Center, Georgia Regents University, Augusta, GA, 30912, USA.
M JainLaboratory of Tumor Angiogenesis, Department of Biochemistry and Molecular Biology, Cancer Center, Georgia Regents University, Augusta, GA, 30912, USA.
H Bagher-EbadianDepartment of Radiology, Henry Ford Health System, Detroit, MI, USA.
B R AchyutLaboratory of Tumor Angiogenesis, Department of Biochemistry and Molecular Biology, Cancer Center, Georgia Regents University, Augusta, GA, 30912, USA.
A S ArbabLaboratory of Tumor Angiogenesis, Department of Biochemistry and Molecular Biology, Cancer Center, Georgia Regents University, Augusta, GA, 30912, USA.
Georgia Regents Medical Center · USAugusta University · 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

Antiangiogenic agents caused paradoxical increase in pro-growth and pro-angiogenic factors and caused tumor growth in glioblastoma (GBM). It is hypothesized that paradoxical increase in pro-angiogenic factors would mobilize Bone Marrow Derived Cells (BMDCs) to the treated tumor and cause refractory tumor growth. The purposes of the studies were to determine whether whole body irradiation (WBIR) or a CXCR4 antagonist (AMD3100) will potentiate the effect of vatalanib (a VEGFR2 tyrosine kinase inhibitor) and prevent the refractory growth of GBM. Human GBM were grown orthotopically in three groups of rats (control, pretreated with WBIR and AMD3100) and randomly selected for vehicle or vatalanib treatments for 2 weeks. Then all animals underwent Magnetic Resonance Imaging (MRI) followed by euthanasia and histochemical analysis. Tumor volume and different vascular parameters (plasma volume (v

Indexed as

bone marrow derived cells (BMDC)CXCR4 antagonist (AMD3100)Glioblastomareceptor tyrosine kinase inhibitor (RTKI)whole body irradiation

Identifiers

PMID27429653
PMCPMC4945124
OpenAlexW2485068381

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.