Central nervous system penetration and enhancement of temozolomide activity in childhood medulloblastoma models by poly(ADP-ribose) polymerase inhibitor AG-014699

Background: Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour. Poly(ADP-ribose) polymerase (PARP) inhibitors enhance temozolomide activity in extracranial adult and paediatric human malignancies. Methods: We assessed the effect of AG-014699, a cli...

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Published inBritish journal of cancer Vol. 103; no. 10; pp. 1588 - 1596
Main Authors Daniel, R A, Rozanska, A L, Mulligan, E A, Drew, Y, Thomas, H D, Castelbuono, D J, Hostomsky, Z, Plummer, E R, Tweddle, D A, Boddy, A V, Clifford, S C, Curtin, N J
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 09.11.2010
Nature Publishing Group
Subjects
631/154/436/1729
631/378/1689/1690
692/308/2778
692/700/565/1436/1437
Animals
Antineoplastic Agents, Alkylating - therapeutic use
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
Brain cancer
Brain research
Cancer Research
Cancer therapies
Cell Division - drug effects
Cell Line, Tumor
Cell Survival - drug effects
Central Nervous System Neoplasms - drug therapy
Central Nervous System Neoplasms - enzymology
Central Nervous System Neoplasms - pathology
Child
Dacarbazine - analogs & derivatives
Dacarbazine - therapeutic use
DNA damage
DNA methylation
DNA Mismatch Repair - drug effects
DNA Repair - drug effects
Drug Resistance
Epidemiology
Humans
Indoles - therapeutic use
Medical research
Medical sciences
Medulloblastoma - drug therapy
Medulloblastoma - enzymology
Medulloblastoma - pathology
Mice
Mice, Nude
Molecular Medicine
Nervous system
Neurology
Oncology
Pediatrics
Poly (ADP-Ribose) Polymerase-1
Poly(ADP-ribose) Polymerase Inhibitors
Protein Serine-Threonine Kinases - antagonists & inhibitors
Temozolomide
Toxicity
Translational Therapeutics
Transplantation, Heterologous
Tumors
Tumors of the nervous system. Phacomatoses
temozolomide
CNS
PARP
xenograft
medulloblastoma
Antineoplastic agent
Glycosyltransferases
Central nervous system
Transplantation
Heterotransplantation
Cancerology
Surgery
ADP-ribosyltransferase
Graft
Child
Human
Nervous system diseases
Enzyme
Transferases
Malignant tumor
Biological activity
Cerebral disorder
NAD
Alkylating agent
Penetration
Treatment
Animal
Medulloblastoma
Central nervous system disease
Inhibitor
Models
Temozolomide
Pentosyltransferases
Cancer
Online AccessGet full text

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Abstract Background: Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour. Poly(ADP-ribose) polymerase (PARP) inhibitors enhance temozolomide activity in extracranial adult and paediatric human malignancies. Methods: We assessed the effect of AG-014699, a clinically active PARP inhibitor, on temozolomide-induced growth inhibition in human medulloblastoma models. Pharmacokinetic, pharmacodynamic and toxicity assays were performed in tumour-bearing mice. Results: Sensitivity to temozolomide in vitro was consistent with methylguanine methyltransferase (MGMT) and DNA mismatch repair (MMR) status; MGMT + MMR + D384Med cells (temozolomide GI 50 =220  μ M ), representative of most primary medulloblastomas, were sensitised fourfold by AG-014699; MGMT − MMR + D425Med cells were hypersensitive (GI 50 =9  μ M ) and not sensitised by AG-014699, whereas MGMT + MMR − temozolomide-resistant D283Med cells (GI 50 =807  μ M ) were sensitised 20-fold. In xenograft models, co-administration of AG-014699 produced an increase in temozolomide-induced tumour growth delay in D384Med xenografts. Consistent with the in vitro data, temozolomide caused complete tumour regressions of D425Med xenografts, whereas D283Med xenografts were relatively resistant. AG-014699 was not toxic, accumulated and reduced PARP activity ⩾75% in xenograft and brain tissues. Conclusion: We show for the first time central nervous system penetration and inhibition of brain PARP activity by AG-014699. Taken together with our in vitro chemosensitisation and toxicity data, these findings support further evaluation of the clinical potential of AG-014699–temozolomide combinations in intra-cranial malignancies.
AbstractList Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour. Poly(ADP-ribose) polymerase (PARP) inhibitors enhance temozolomide activity in extracranial adult and paediatric human malignancies.BACKGROUNDTemozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour. Poly(ADP-ribose) polymerase (PARP) inhibitors enhance temozolomide activity in extracranial adult and paediatric human malignancies.We assessed the effect of AG-014699, a clinically active PARP inhibitor, on temozolomide-induced growth inhibition in human medulloblastoma models. Pharmacokinetic, pharmacodynamic and toxicity assays were performed in tumour-bearing mice.METHODSWe assessed the effect of AG-014699, a clinically active PARP inhibitor, on temozolomide-induced growth inhibition in human medulloblastoma models. Pharmacokinetic, pharmacodynamic and toxicity assays were performed in tumour-bearing mice.Sensitivity to temozolomide in vitro was consistent with methylguanine methyltransferase (MGMT) and DNA mismatch repair (MMR) status; MGMT(+) MMR(+) D384Med cells (temozolomide GI(50)=220 μM), representative of most primary medulloblastomas, were sensitised fourfold by AG-014699; MGMT⁻ MMR(+) D425Med cells were hypersensitive (GI(50)=9 μM) and not sensitised by AG-014699, whereas MGMT(+) MMR⁻ temozolomide-resistant D283Med cells (GI₅₀=807 μM) were sensitised 20-fold. In xenograft models, co-administration of AG-014699 produced an increase in temozolomide-induced tumour growth delay in D384Med xenografts. Consistent with the in vitro data, temozolomide caused complete tumour regressions of D425Med xenografts, whereas D283Med xenografts were relatively resistant. AG-014699 was not toxic, accumulated and reduced PARP activity ≥75% in xenograft and brain tissues.RESULTSSensitivity to temozolomide in vitro was consistent with methylguanine methyltransferase (MGMT) and DNA mismatch repair (MMR) status; MGMT(+) MMR(+) D384Med cells (temozolomide GI(50)=220 μM), representative of most primary medulloblastomas, were sensitised fourfold by AG-014699; MGMT⁻ MMR(+) D425Med cells were hypersensitive (GI(50)=9 μM) and not sensitised by AG-014699, whereas MGMT(+) MMR⁻ temozolomide-resistant D283Med cells (GI₅₀=807 μM) were sensitised 20-fold. In xenograft models, co-administration of AG-014699 produced an increase in temozolomide-induced tumour growth delay in D384Med xenografts. Consistent with the in vitro data, temozolomide caused complete tumour regressions of D425Med xenografts, whereas D283Med xenografts were relatively resistant. AG-014699 was not toxic, accumulated and reduced PARP activity ≥75% in xenograft and brain tissues.We show for the first time central nervous system penetration and inhibition of brain PARP activity by AG-014699. Taken together with our in vitro chemosensitisation and toxicity data, these findings support further evaluation of the clinical potential of AG-014699-temozolomide combinations in intra-cranial malignancies.CONCLUSIONWe show for the first time central nervous system penetration and inhibition of brain PARP activity by AG-014699. Taken together with our in vitro chemosensitisation and toxicity data, these findings support further evaluation of the clinical potential of AG-014699-temozolomide combinations in intra-cranial malignancies.
Background:Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour. Poly(ADP-ribose) polymerase (PARP) inhibitors enhance temozolomide activity in extracranial adult and paediatric human malignancies. Methods:We assessed the effect of AG-014699, a clinically active PARP inhibitor, on temozolomide-induced growth inhibition in human medulloblastoma models. Pharmacokinetic, pharmacodynamic and toxicity assays were performed in tumour-bearing mice. Results:Sensitivity to temozolomide in vitro was consistent with methylguanine methyltransferase (MGMT) and DNA mismatch repair (MMR) status; MGMT super(+) MMR super(+) D384Med cells (temozolomide GI sub(50)=220 mu M), representative of most primary medulloblastomas, were sensitised fourfold by AG-014699; MGMT super(-) MMR super(+) D425Med cells were hypersensitive (GI sub(50)=9 mu M) and not sensitised by AG-014699, whereas MGMT super(+) MMR super(-) temozolomide-resistant D283Med cells (GI sub(50)=807 mu M) were sensitised 20-fold. In xenograft models, co-administration of AG-014699 produced an increase in temozolomide-induced tumour growth delay in D384Med xenografts. Consistent with the in vitro data, temozolomide caused complete tumour regressions of D425Med xenografts, whereas D283Med xenografts were relatively resistant. AG-014699 was not toxic, accumulated and reduced PARP activity greater than or equal to 75% in xenograft and brain tissues. Conclusion:We show for the first time central nervous system penetration and inhibition of brain PARP activity by AG-014699. Taken together with our in vitro chemosensitisation and toxicity data, these findings support further evaluation of the clinical potential of AG-014699-temozolomide combinations in intra-cranial malignancies.
Background: Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour. Poly(ADP-ribose) polymerase (PARP) inhibitors enhance temozolomide activity in extracranial adult and paediatric human malignancies. Methods: We assessed the effect of AG-014699, a clinically active PARP inhibitor, on temozolomide-induced growth inhibition in human medulloblastoma models. Pharmacokinetic, pharmacodynamic and toxicity assays were performed in tumour-bearing mice. Results: Sensitivity to temozolomide in vitro was consistent with methylguanine methyltransferase (MGMT) and DNA mismatch repair (MMR) status; MGMT + MMR + D384Med cells (temozolomide GI 50 =220  μ M ), representative of most primary medulloblastomas, were sensitised fourfold by AG-014699; MGMT − MMR + D425Med cells were hypersensitive (GI 50 =9  μ M ) and not sensitised by AG-014699, whereas MGMT + MMR − temozolomide-resistant D283Med cells (GI 50 =807  μ M ) were sensitised 20-fold. In xenograft models, co-administration of AG-014699 produced an increase in temozolomide-induced tumour growth delay in D384Med xenografts. Consistent with the in vitro data, temozolomide caused complete tumour regressions of D425Med xenografts, whereas D283Med xenografts were relatively resistant. AG-014699 was not toxic, accumulated and reduced PARP activity ⩾75% in xenograft and brain tissues. Conclusion: We show for the first time central nervous system penetration and inhibition of brain PARP activity by AG-014699. Taken together with our in vitro chemosensitisation and toxicity data, these findings support further evaluation of the clinical potential of AG-014699–temozolomide combinations in intra-cranial malignancies.
Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour. Poly(ADP-ribose) polymerase (PARP) inhibitors enhance temozolomide activity in extracranial adult and paediatric human malignancies. We assessed the effect of AG-014699, a clinically active PARP inhibitor, on temozolomide-induced growth inhibition in human medulloblastoma models. Pharmacokinetic, pharmacodynamic and toxicity assays were performed in tumour-bearing mice. Sensitivity to temozolomide in vitro was consistent with methylguanine methyltransferase (MGMT) and DNA mismatch repair (MMR) status; MGMT(+) MMR(+) D384Med cells (temozolomide GI(50)=220 μM), representative of most primary medulloblastomas, were sensitised fourfold by AG-014699; MGMT⁻ MMR(+) D425Med cells were hypersensitive (GI(50)=9 μM) and not sensitised by AG-014699, whereas MGMT(+) MMR⁻ temozolomide-resistant D283Med cells (GI₅₀=807 μM) were sensitised 20-fold. In xenograft models, co-administration of AG-014699 produced an increase in temozolomide-induced tumour growth delay in D384Med xenografts. Consistent with the in vitro data, temozolomide caused complete tumour regressions of D425Med xenografts, whereas D283Med xenografts were relatively resistant. AG-014699 was not toxic, accumulated and reduced PARP activity ≥75% in xenograft and brain tissues. We show for the first time central nervous system penetration and inhibition of brain PARP activity by AG-014699. Taken together with our in vitro chemosensitisation and toxicity data, these findings support further evaluation of the clinical potential of AG-014699-temozolomide combinations in intra-cranial malignancies.
Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour. Poly(ADP-ribose) polymerase (PARP) inhibitors enhance temozolomide activity in extracranial adult and paediatric human malignancies. We assessed the effect of AG-014699, a clinically active PARP inhibitor, on temozolomide-induced growth inhibition in human medulloblastoma models. Pharmacokinetic, pharmacodynamic and toxicity assays were performed in tumour-bearing mice. Sensitivity to temozolomide in vitro was consistent with methylguanine methyltransferase (MGMT) and DNA mismatch repair (MMR) status; MGMT(+) MMR(+) D384Med cells (temozolomide GI(50)=220μM), representative of most primary medulloblastomas, were sensitised fourfold by AG-014699; MGMT MMR(+) D425Med cells were hypersensitive (GI(50)=9μM) and not sensitised by AG-014699, whereas MGMT(+) MMR temozolomide-resistant D283Med cells (GI=807μM) were sensitised 20-fold. In xenograft models, co-administration of AG-014699 produced an increase in temozolomide-induced tumour growth delay in D384Med xenografts. Consistent with the in vitro data, temozolomide caused complete tumour regressions of D425Med xenografts, whereas D283Med xenografts were relatively resistant. AG-014699 was not toxic, accumulated and reduced PARP activity ≥75% in xenograft and brain tissues. We show for the first time central nervous system penetration and inhibition of brain PARP activity by AG-014699. Taken together with our in vitro chemosensitisation and toxicity data, these findings support further evaluation of the clinical potential of AG-014699-temozolomide combinations in intra-cranial malignancies.
Author Rozanska, A L
Plummer, E R
Boddy, A V
Daniel, R A
Drew, Y
Thomas, H D
Mulligan, E A
Curtin, N J
Castelbuono, D J
Hostomsky, Z
Clifford, S C
Tweddle, D A
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ContentType Journal Article
Copyright The Author(s) 2010
2015 INIST-CNRS
Copyright Nature Publishing Group Nov 9, 2010
Copyright © 2010 Cancer Research UK 2010 Cancer Research UK
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Issue 10
Keywords temozolomide
CNS
PARP
xenograft
medulloblastoma
Antineoplastic agent
Glycosyltransferases
Central nervous system
Transplantation
Heterotransplantation
Cancerology
Surgery
ADP-ribosyltransferase
Graft
Child
Human
Nervous system diseases
Enzyme
Transferases
Malignant tumor
Biological activity
Cerebral disorder
NAD
Alkylating agent
Penetration
Treatment
Animal
Medulloblastoma
Central nervous system disease
Inhibitor
Models
Temozolomide
Pentosyltransferases
Cancer
Language English
License CC BY 4.0
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CH Wang (BF6605946_CR33) 2009; 25
R Plummer (BF6605946_CR26) 2008; 14
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M Ali (BF6605946_CR1) 2009; 15
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A Broniscer (BF6605946_CR4) 2007; 13
NJ Curtin (BF6605946_CR7) 2007; 11
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MM Mrugala (BF6605946_CR21) 2008; 5
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P Jagtap (BF6605946_CR16) 2005; 4
CL Cheng (BF6605946_CR6) 2005; 4
B Pizer (BF6605946_CR23) 2008; 93
HS Friedman (BF6605946_CR13) 1995; 55
M Viana-Pereira (BF6605946_CR32) 2009; 11
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SSID ssj0009087
Score 2.2837188
Snippet Background: Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour. Poly(ADP-ribose) polymerase (PARP)...
Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour. Poly(ADP-ribose) polymerase (PARP) inhibitors enhance...
Background:Temozolomide shows activity against medulloblastoma, the most common malignant paediatric brain tumour. Poly(ADP-ribose) polymerase (PARP)...
SourceID pubmedcentral
proquest
crossref
pubmed
pascalfrancis
springer
nature
SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage 1588
SubjectTerms 631/154/436/1729
631/378/1689/1690
692/308/2778
692/700/565/1436/1437
Animals
Antineoplastic Agents, Alkylating - therapeutic use
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
Brain cancer
Brain research
Cancer Research
Cancer therapies
Cell Division - drug effects
Cell Line, Tumor
Cell Survival - drug effects
Central Nervous System Neoplasms - drug therapy
Central Nervous System Neoplasms - enzymology
Central Nervous System Neoplasms - pathology
Child
Dacarbazine - analogs & derivatives
Dacarbazine - therapeutic use
DNA damage
DNA methylation
DNA Mismatch Repair - drug effects
DNA Repair - drug effects
Drug Resistance
Epidemiology
Humans
Indoles - therapeutic use
Medical research
Medical sciences
Medulloblastoma - drug therapy
Medulloblastoma - enzymology
Medulloblastoma - pathology
Mice
Mice, Nude
Molecular Medicine
Nervous system
Neurology
Oncology
Pediatrics
Poly (ADP-Ribose) Polymerase-1
Poly(ADP-ribose) Polymerase Inhibitors
Protein Serine-Threonine Kinases - antagonists & inhibitors
Temozolomide
Toxicity
Translational Therapeutics
Transplantation, Heterologous
Tumors
Tumors of the nervous system. Phacomatoses
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Title Central nervous system penetration and enhancement of temozolomide activity in childhood medulloblastoma models by poly(ADP-ribose) polymerase inhibitor AG-014699
URI http://dx.doi.org/10.1038/sj.bjc.6605946
https://link.springer.com/article/10.1038/sj.bjc.6605946
https://www.ncbi.nlm.nih.gov/pubmed/20978505
https://www.proquest.com/docview/763657910
https://www.proquest.com/docview/763473794/abstract/
https://search.proquest.com/docview/954608629
https://pubmed.ncbi.nlm.nih.gov/PMC2990587
Volume 103
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