Effects of tyrosine kinase inhibitors and CXCR4 antagonist on tumor growth and angiogenesis in rat glioma model: MRI and protein analysis study

Meser M. Ali, Sanath Kumar, Adarsh Shankar, Nadimpalli R.S. Varma, A. S.M. Iskander, Branislava Janic, Wilson B. Chwang, Rajan Jain, Abbas Babajani-Feremi, Thaiz F. Borin, Hassan Bagher-Ebadian, Stephen L. Brown, James R. Ewing, Ali S. Arbab

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

The aim of the study was to determine the antiangiogenic efficacy of vatalanib, sunitinib, and AMD3100 in an animal model of human glioblastoma (GBM) by using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and tumor protein expression analysis. Orthotopic GBM-bearing animals were randomly assigned either to control group or vatalanib, sunitinib, and AMD3100 treatment groups. Following 2 weeks of drug treatment, tumor growth and vascular parameters were measured using DCE-MRI. Expression of different angiogenic factors in tumor extracts was measured using a membrane-based human antibody array kit. Tumor angiogenesis and invasion were determined by immunohistochemistry. DCE-MRI showed a significant increase in tumor size after vatalanib treatment. AMD3100-treated group showed a significant decrease in a number of vascular parameters determined by DCE-MRI. AMD3100 significantly decreased the expression of different angiogenic factors compared to sunitinib or vatalanib; however, there were no significant changes in vascular density among the groups. Sunitinib-treated animals showed significantly higher migration of the invasive cells, whereas in both vatalanib- and AMD3100-treated animals the invasive cell migration distance was significantly lower compared to that of control. Vatalanib and sunitinib resulted in suboptimal therapeutic effect, but AMD3100 treatment resulted in a significant reduction in tumor growth, permeability, interstitial space volume, and invasion of tumor cells in an animal model of GBM.

Original languageEnglish (US)
Pages (from-to)660-669
Number of pages10
JournalTranslational Oncology
Volume6
Issue number6
DOIs
StatePublished - Jan 1 2013

Fingerprint

Glioma
Protein-Tyrosine Kinases
Glioblastoma
Growth
Magnetic Resonance Imaging
Blood Vessels
Neoplasms
Proteins
Angiogenesis Inducing Agents
Cell Movement
Animal Models
Therapeutic Uses
Therapeutics
Tumor Burden
vatalanib
JM 3100
Permeability
Immunohistochemistry
sunitinib
Control Groups

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Effects of tyrosine kinase inhibitors and CXCR4 antagonist on tumor growth and angiogenesis in rat glioma model : MRI and protein analysis study. / Ali, Meser M.; Kumar, Sanath; Shankar, Adarsh; Varma, Nadimpalli R.S.; Iskander, A. S.M.; Janic, Branislava; Chwang, Wilson B.; Jain, Rajan; Babajani-Feremi, Abbas; Borin, Thaiz F.; Bagher-Ebadian, Hassan; Brown, Stephen L.; Ewing, James R.; Arbab, Ali S.

In: Translational Oncology, Vol. 6, No. 6, 01.01.2013, p. 660-669.

Research output: Contribution to journalArticle

Ali, MM, Kumar, S, Shankar, A, Varma, NRS, Iskander, ASM, Janic, B, Chwang, WB, Jain, R, Babajani-Feremi, A, Borin, TF, Bagher-Ebadian, H, Brown, SL, Ewing, JR & Arbab, AS 2013, 'Effects of tyrosine kinase inhibitors and CXCR4 antagonist on tumor growth and angiogenesis in rat glioma model: MRI and protein analysis study', Translational Oncology, vol. 6, no. 6, pp. 660-669. https://doi.org/10.1593/tlo.13559
Ali, Meser M. ; Kumar, Sanath ; Shankar, Adarsh ; Varma, Nadimpalli R.S. ; Iskander, A. S.M. ; Janic, Branislava ; Chwang, Wilson B. ; Jain, Rajan ; Babajani-Feremi, Abbas ; Borin, Thaiz F. ; Bagher-Ebadian, Hassan ; Brown, Stephen L. ; Ewing, James R. ; Arbab, Ali S. / Effects of tyrosine kinase inhibitors and CXCR4 antagonist on tumor growth and angiogenesis in rat glioma model : MRI and protein analysis study. In: Translational Oncology. 2013 ; Vol. 6, No. 6. pp. 660-669.
@article{84b82ca08efb4cc0ac6ade0de5f0473e,
title = "Effects of tyrosine kinase inhibitors and CXCR4 antagonist on tumor growth and angiogenesis in rat glioma model: MRI and protein analysis study",
abstract = "The aim of the study was to determine the antiangiogenic efficacy of vatalanib, sunitinib, and AMD3100 in an animal model of human glioblastoma (GBM) by using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and tumor protein expression analysis. Orthotopic GBM-bearing animals were randomly assigned either to control group or vatalanib, sunitinib, and AMD3100 treatment groups. Following 2 weeks of drug treatment, tumor growth and vascular parameters were measured using DCE-MRI. Expression of different angiogenic factors in tumor extracts was measured using a membrane-based human antibody array kit. Tumor angiogenesis and invasion were determined by immunohistochemistry. DCE-MRI showed a significant increase in tumor size after vatalanib treatment. AMD3100-treated group showed a significant decrease in a number of vascular parameters determined by DCE-MRI. AMD3100 significantly decreased the expression of different angiogenic factors compared to sunitinib or vatalanib; however, there were no significant changes in vascular density among the groups. Sunitinib-treated animals showed significantly higher migration of the invasive cells, whereas in both vatalanib- and AMD3100-treated animals the invasive cell migration distance was significantly lower compared to that of control. Vatalanib and sunitinib resulted in suboptimal therapeutic effect, but AMD3100 treatment resulted in a significant reduction in tumor growth, permeability, interstitial space volume, and invasion of tumor cells in an animal model of GBM.",
author = "Ali, {Meser M.} and Sanath Kumar and Adarsh Shankar and Varma, {Nadimpalli R.S.} and Iskander, {A. S.M.} and Branislava Janic and Chwang, {Wilson B.} and Rajan Jain and Abbas Babajani-Feremi and Borin, {Thaiz F.} and Hassan Bagher-Ebadian and Brown, {Stephen L.} and Ewing, {James R.} and Arbab, {Ali S.}",
year = "2013",
month = "1",
day = "1",
doi = "10.1593/tlo.13559",
language = "English (US)",
volume = "6",
pages = "660--669",
journal = "Translational Oncology",
issn = "1936-5233",
publisher = "Neoplasia Press",
number = "6",

}

TY - JOUR

T1 - Effects of tyrosine kinase inhibitors and CXCR4 antagonist on tumor growth and angiogenesis in rat glioma model

T2 - MRI and protein analysis study

AU - Ali, Meser M.

AU - Kumar, Sanath

AU - Shankar, Adarsh

AU - Varma, Nadimpalli R.S.

AU - Iskander, A. S.M.

AU - Janic, Branislava

AU - Chwang, Wilson B.

AU - Jain, Rajan

AU - Babajani-Feremi, Abbas

AU - Borin, Thaiz F.

AU - Bagher-Ebadian, Hassan

AU - Brown, Stephen L.

AU - Ewing, James R.

AU - Arbab, Ali S.

PY - 2013/1/1

Y1 - 2013/1/1

N2 - The aim of the study was to determine the antiangiogenic efficacy of vatalanib, sunitinib, and AMD3100 in an animal model of human glioblastoma (GBM) by using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and tumor protein expression analysis. Orthotopic GBM-bearing animals were randomly assigned either to control group or vatalanib, sunitinib, and AMD3100 treatment groups. Following 2 weeks of drug treatment, tumor growth and vascular parameters were measured using DCE-MRI. Expression of different angiogenic factors in tumor extracts was measured using a membrane-based human antibody array kit. Tumor angiogenesis and invasion were determined by immunohistochemistry. DCE-MRI showed a significant increase in tumor size after vatalanib treatment. AMD3100-treated group showed a significant decrease in a number of vascular parameters determined by DCE-MRI. AMD3100 significantly decreased the expression of different angiogenic factors compared to sunitinib or vatalanib; however, there were no significant changes in vascular density among the groups. Sunitinib-treated animals showed significantly higher migration of the invasive cells, whereas in both vatalanib- and AMD3100-treated animals the invasive cell migration distance was significantly lower compared to that of control. Vatalanib and sunitinib resulted in suboptimal therapeutic effect, but AMD3100 treatment resulted in a significant reduction in tumor growth, permeability, interstitial space volume, and invasion of tumor cells in an animal model of GBM.

AB - The aim of the study was to determine the antiangiogenic efficacy of vatalanib, sunitinib, and AMD3100 in an animal model of human glioblastoma (GBM) by using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and tumor protein expression analysis. Orthotopic GBM-bearing animals were randomly assigned either to control group or vatalanib, sunitinib, and AMD3100 treatment groups. Following 2 weeks of drug treatment, tumor growth and vascular parameters were measured using DCE-MRI. Expression of different angiogenic factors in tumor extracts was measured using a membrane-based human antibody array kit. Tumor angiogenesis and invasion were determined by immunohistochemistry. DCE-MRI showed a significant increase in tumor size after vatalanib treatment. AMD3100-treated group showed a significant decrease in a number of vascular parameters determined by DCE-MRI. AMD3100 significantly decreased the expression of different angiogenic factors compared to sunitinib or vatalanib; however, there were no significant changes in vascular density among the groups. Sunitinib-treated animals showed significantly higher migration of the invasive cells, whereas in both vatalanib- and AMD3100-treated animals the invasive cell migration distance was significantly lower compared to that of control. Vatalanib and sunitinib resulted in suboptimal therapeutic effect, but AMD3100 treatment resulted in a significant reduction in tumor growth, permeability, interstitial space volume, and invasion of tumor cells in an animal model of GBM.

UR - http://www.scopus.com/inward/record.url?scp=84891685345&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84891685345&partnerID=8YFLogxK

U2 - 10.1593/tlo.13559

DO - 10.1593/tlo.13559

M3 - Article

AN - SCOPUS:84891685345

VL - 6

SP - 660

EP - 669

JO - Translational Oncology

JF - Translational Oncology

SN - 1936-5233

IS - 6

ER -