K27M mutation in histone H3.3 defines clinically and biologically distinct subgroups of pediatric diffuse intrinsic pontine gliomas

Pediatric glioblastomas (GBM) including diffuse intrinsic pontine gliomas (DIPG) are devastating brain tumors with no effective therapy. Here, we investigated clinical and biological impacts of histone H3.3 mutations. Forty-two DIPGs were tested for H3.3 mutations. Wild-type versus mutated (K27M-H3....

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Veröffentlicht in:Acta neuropathologica Jg. 124; H. 3; S. 439 - 447
Hauptverfasser: Khuong-Quang, Dong-Anh, Buczkowicz, Pawel, Rakopoulos, Patricia, Liu, Xiao-Yang, Fontebasso, Adam M., Bouffet, Eric, Bartels, Ute, Albrecht, Steffen, Schwartzentruber, Jeremy, Letourneau, Louis, Bourgey, Mathieu, Bourque, Guillaume, Montpetit, Alexandre, Bourret, Genevieve, Lepage, Pierre, Fleming, Adam, Lichter, Peter, Kool, Marcel, von Deimling, Andreas, Sturm, Dominik, Korshunov, Andrey, Faury, Damien, Jones, David T., Majewski, Jacek, Pfister, Stefan M., Jabado, Nada, Hawkins, Cynthia
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Berlin/Heidelberg Springer-Verlag 01.09.2012
Springer
Springer Nature B.V
Schlagworte:
Adolescent
Algorithms
Biopsy
Brain cancer
Brain research
Brain stem
Brain Stem Neoplasms - genetics
Brain Stem Neoplasms - mortality
Brain Stem Neoplasms - pathology
Brain tumors
Cancer research
Cancer therapies
Child
Child, Preschool
Children
Clinical trials
Comparative analysis
copy number
Cortex
Decision making
Female
Gene Expression Profiling
Genetic aspects
Glioblastoma
Glioma
Glioma - genetics
Glioma - mortality
Glioma - pathology
Gliomas
Histones
Histones - genetics
Hospitals
Humans
Infant
Kinases
Male
Medical research
Medicine
Medicine & Public Health
Mutation
Myc protein
Neurosciences
Original Paper
p53 protein
Pathology
Pediatrics
Platelet-derived growth factor
Pons - pathology
Prognosis
Survival
Survival Rate
Tumor proteins
Tumors
Canada
Montreal Quebec Canada
Germany
H3.3
DIPG
Targeted therapy
TP53
Survival
ATRX
ISSN:0001-6322, 1432-0533, 1432-0533
Online-Zugang:Volltext
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Abstract Pediatric glioblastomas (GBM) including diffuse intrinsic pontine gliomas (DIPG) are devastating brain tumors with no effective therapy. Here, we investigated clinical and biological impacts of histone H3.3 mutations. Forty-two DIPGs were tested for H3.3 mutations. Wild-type versus mutated (K27M-H3.3) subgroups were compared for HIST1H3B , IDH , ATRX and TP53 mutations, copy number alterations and clinical outcome. K27M-H3.3 occurred in 71 %, TP53 mutations in 77 % and ATRX mutations in 9 % of DIPGs. ATRX mutations were more frequent in older children ( p  < 0.0001). No G34V/R-H3.3, IDH1/2 or H3.1 mutations were identified. K27M-H3.3 DIPGs showed specific copy number changes, including all gains/amplifications of PDGFRA and MYC/PVT1 loci. Notably, all long-term survivors were H3.3 wild type and this group of patients had better overall survival. K27M-H3.3 mutation defines clinically and biologically distinct subgroups and is prevalent in DIPG, which will impact future therapeutic trial design. K27M- and G34V-H3.3 have location-based incidence (brainstem/cortex) and potentially play distinct roles in pediatric GBM pathogenesis. K27M-H3.3 is universally associated with short survival in DIPG, while patients wild-type for H3.3 show improved survival. Based on prognostic and therapeutic implications, our findings argue for H3.3-mutation testing at diagnosis, which should be rapidly integrated into the clinical decision-making algorithm, particularly in atypical DIPG.
AbstractList Pediatric glioblastomas (GBM) including diffuse intrinsic pontine gliomas (DIPG) are devastating brain tumors with no effective therapy. Here, we investigated clinical and biological impacts of histone H3.3 mutations. Forty-two DIPGs were tested for H3.3 mutations. Wild-type versus mutated (K27M-H3.3) subgroups were compared for HIST1H3B, IDH, ATRX and TP53 mutations, copy number alterations and clinical outcome. K27M-H3.3 occurred in 71 %, TP53 mutations in 77 % and ATRX mutations in 9 % of DIPGs. ATRX mutations were more frequent in older children (p < 0.0001). No G34V/R-H3.3, IDH1/2 or H3.1 mutations were identified. K27M-H3.3 DIPGs showed specific copy number changes, including all gains/amplifications of PDGFRA and MYC/PVT1 loci. Notably, all long-term survivors were H3.3 wild type and this group of patients had better overall survival. K27M-H3.3 mutation defines clinically and biologically distinct subgroups and is prevalent in DIPG, which will impact future therapeutic trial design. K27M- and G34V-H3.3 have location-based incidence (brainstem/cortex) and potentially play distinct roles in pediatric GBM pathogenesis. K27M-H3.3 is universally associated with short survival in DIPG, while patients wild-type for H3.3 show improved survival. Based on prognostic and therapeutic implications, our findings argue for H3.3-mutation testing at diagnosis, which should be rapidly integrated into the clinical decision-making algorithm, particularly in atypical DIPG.
Pediatric glioblastomas (GBM) including diffuse intrinsic pontine gliomas (DIPG) are devastating brain tumors with no effective therapy. Here, we investigated clinical and biological impacts of histone H3.3 mutations. Forty-two DIPGs were tested for H3.3 mutations. Wildtype versus mutated (K27M-H3.3) subgroups were compared for HIST1H3B, IDH, ATRX and TP53 mutations, copy number alterations and clinical outcome. K27M-H3.3 occurred in 71%, TP53 mutations in 77% and ATRX mutations in 9% of DIPGs. ATRX mutations were more frequent in older children (p < 0.0001). No G34V/R-H3.3, IDH1/2 or H3.1 mutations were identified. K27M-H3.3 DIPGs showed specific copy number changes, including all gains/amplifications of PDGFRA and MYC/PVT1 loci. Notably, all long-term survivors were H3.3 wild type and this group of patients had better overall survival. K27MH3.3 mutation defines clinically and biologically distinct subgroups and is prevalent in DIPG, which will impact future therapeutic trial design. K27M-and G34V-H3.3 have location-based incidence (brainstem/cortex) and potentially play distinct roles in pediatric GBM pathogenesis. K27M-H3.3 is universally associated with short survival in DIPG, while patients wild-type for H3.3 show improved survival. Based on prognostic and therapeutic implications, our findings argue for H3.3-mutation testing at diagnosis, which should be rapidly integrated into the clinical decision-making algorithm, particularly in atypical DIPG. Keywords DIPG * H3.3 * ATRX * TP53 * Survival * Targeted therapy
Pediatric glioblastomas (GBM) including diffuse intrinsic pontine gliomas (DIPG) are devastating brain tumors with no effective therapy. Here, we investigated clinical and biological impacts of histone H3.3 mutations. Forty-two DIPGs were tested for H3.3 mutations. Wild-type versus mutated (K27M-H3.3) subgroups were compared for HIST1H3B, IDH, ATRX and TP53 mutations, copy number alterations and clinical outcome. K27M-H3.3 occurred in 71 %, TP53 mutations in 77 % and ATRX mutations in 9 % of DIPGs. ATRX mutations were more frequent in older children (p < 0.0001). No G34V/R-H3.3, IDH1/2 or H3.1 mutations were identified. K27M-H3.3 DIPGs showed specific copy number changes, including all gains/amplifications of PDGFRA and MYC/PVT1 loci. Notably, all long-term survivors were H3.3 wild type and this group of patients had better overall survival. K27M-H3.3 mutation defines clinically and biologically distinct subgroups and is prevalent in DIPG, which will impact future therapeutic trial design. K27M- and G34V-H3.3 have location-based incidence (brainstem/cortex) and potentially play distinct roles in pediatric GBM pathogenesis. K27M-H3.3 is universally associated with short survival in DIPG, while patients wild-type for H3.3 show improved survival. Based on prognostic and therapeutic implications, our findings argue for H3.3-mutation testing at diagnosis, which should be rapidly integrated into the clinical decision-making algorithm, particularly in atypical DIPG.
Pediatric glioblastomas (GBM) including diffuse intrinsic pontine gliomas (DIPG) are devastating brain tumors with no effective therapy. Here, we investigated clinical and biological impacts of histone H3.3 mutations. Forty-two DIPGs were tested for H3.3 mutations. Wildtype versus mutated (K27M-H3.3) subgroups were compared for HIST1H3B, IDH, ATRX and TP53 mutations, copy number alterations and clinical outcome. K27M-H3.3 occurred in 71%, TP53 mutations in 77% and ATRX mutations in 9% of DIPGs. ATRX mutations were more frequent in older children (p < 0.0001). No G34V/R-H3.3, IDH1/2 or H3.1 mutations were identified. K27M-H3.3 DIPGs showed specific copy number changes, including all gains/amplifications of PDGFRA and MYC/PVT1 loci. Notably, all long-term survivors were H3.3 wild type and this group of patients had better overall survival. K27MH3.3 mutation defines clinically and biologically distinct subgroups and is prevalent in DIPG, which will impact future therapeutic trial design. K27M-and G34V-H3.3 have location-based incidence (brainstem/cortex) and potentially play distinct roles in pediatric GBM pathogenesis. K27M-H3.3 is universally associated with short survival in DIPG, while patients wild-type for H3.3 show improved survival. Based on prognostic and therapeutic implications, our findings argue for H3.3-mutation testing at diagnosis, which should be rapidly integrated into the clinical decision-making algorithm, particularly in atypical DIPG.
Pediatric glioblastomas (GBM) including diffuse intrinsic pontine gliomas (DIPG) are devastating brain tumors with no effective therapy. Here, we investigated clinical and biological impacts of histone H3.3 mutations. Forty-two DIPGs were tested for H3.3 mutations. Wild-type versus mutated (K27M-H3.3) subgroups were compared for HIST1H3B, IDH, ATRX and TP53 mutations, copy number alterations and clinical outcome. K27M-H3.3 occurred in 71 %, TP53 mutations in 77 % and ATRX mutations in 9 % of DIPGs. ATRX mutations were more frequent in older children (p < 0.0001). No G34V/R-H3.3, IDH1/2 or H3.1 mutations were identified. K27M-H3.3 DIPGs showed specific copy number changes, including all gains/amplifications of PDGFRA and MYC/PVT1 loci. Notably, all long-term survivors were H3.3 wild type and this group of patients had better overall survival. K27M-H3.3 mutation defines clinically and biologically distinct subgroups and is prevalent in DIPG, which will impact future therapeutic trial design. K27M- and G34V-H3.3 have location-based incidence (brainstem/cortex) and potentially play distinct roles in pediatric GBM pathogenesis. K27M-H3.3 is universally associated with short survival in DIPG, while patients wild-type for H3.3 show improved survival. Based on prognostic and therapeutic implications, our findings argue for H3.3-mutation testing at diagnosis, which should be rapidly integrated into the clinical decision-making algorithm, particularly in atypical DIPG.Pediatric glioblastomas (GBM) including diffuse intrinsic pontine gliomas (DIPG) are devastating brain tumors with no effective therapy. Here, we investigated clinical and biological impacts of histone H3.3 mutations. Forty-two DIPGs were tested for H3.3 mutations. Wild-type versus mutated (K27M-H3.3) subgroups were compared for HIST1H3B, IDH, ATRX and TP53 mutations, copy number alterations and clinical outcome. K27M-H3.3 occurred in 71 %, TP53 mutations in 77 % and ATRX mutations in 9 % of DIPGs. ATRX mutations were more frequent in older children (p < 0.0001). No G34V/R-H3.3, IDH1/2 or H3.1 mutations were identified. K27M-H3.3 DIPGs showed specific copy number changes, including all gains/amplifications of PDGFRA and MYC/PVT1 loci. Notably, all long-term survivors were H3.3 wild type and this group of patients had better overall survival. K27M-H3.3 mutation defines clinically and biologically distinct subgroups and is prevalent in DIPG, which will impact future therapeutic trial design. K27M- and G34V-H3.3 have location-based incidence (brainstem/cortex) and potentially play distinct roles in pediatric GBM pathogenesis. K27M-H3.3 is universally associated with short survival in DIPG, while patients wild-type for H3.3 show improved survival. Based on prognostic and therapeutic implications, our findings argue for H3.3-mutation testing at diagnosis, which should be rapidly integrated into the clinical decision-making algorithm, particularly in atypical DIPG.
Pediatric glioblastomas (GBM) including diffuse intrinsic pontine gliomas (DIPG) are devastating brain tumors with no effective therapy. Here, we investigated clinical and biological impacts of histone H3.3 mutations. Forty-two DIPGs were tested for H3.3 mutations. Wild-type versus mutated (K27M-H3.3) subgroups were compared for HIST1H3B, IDH, ATRX and TP53 mutations, copy number alterations and clinical outcome. K27M-H3.3 occurred in 71 %, TP53 mutations in 77 % and ATRX mutations in 9 % of DIPGs. ATRX mutations were more frequent in older children (p < 0.0001). No G34V/R-H3.3, IDH1/2 or H3.1 mutations were identified. K27M-H3.3 DIPGs showed specific copy number changes, including all gains/amplifications of PDGFRA and MYC/PVT1 loci. Notably, all long-term survivors were H3.3 wild type and this group of patients had better overall survival. K27M-H3.3 mutation defines clinically and biologically distinct subgroups and is prevalent in DIPG, which will impact future therapeutic trial design. K27M- and G34V-H3.3 have location-based incidence (brainstem/cortex) and potentially play distinct roles in pediatric GBM pathogenesis. K27M-H3.3 is universally associated with short survival in DIPG, while patients wild-type for H3.3 show improved survival. Based on prognostic and therapeutic implications, our findings argue for H3.3-mutation testing at diagnosis, which should be rapidly integrated into the clinical decision-making algorithm, particularly in atypical DIPG.[PUBLICATION ABSTRACT]
Pediatric glioblastomas (GBM) including diffuse intrinsic pontine gliomas (DIPG) are devastating brain tumors with no effective therapy. Here, we investigated clinical and biological impacts of histone H3.3 mutations. Forty-two DIPGs were tested for H3.3 mutations. Wild-type versus mutated (K27M-H3.3) subgroups were compared for HIST1H3B , IDH , ATRX and TP53 mutations, copy number alterations and clinical outcome. K27M-H3.3 occurred in 71 %, TP53 mutations in 77 % and ATRX mutations in 9 % of DIPGs. ATRX mutations were more frequent in older children ( p  < 0.0001). No G34V/R-H3.3, IDH1/2 or H3.1 mutations were identified. K27M-H3.3 DIPGs showed specific copy number changes, including all gains/amplifications of PDGFRA and MYC/PVT1 loci. Notably, all long-term survivors were H3.3 wild type and this group of patients had better overall survival. K27M-H3.3 mutation defines clinically and biologically distinct subgroups and is prevalent in DIPG, which will impact future therapeutic trial design. K27M- and G34V-H3.3 have location-based incidence (brainstem/cortex) and potentially play distinct roles in pediatric GBM pathogenesis. K27M-H3.3 is universally associated with short survival in DIPG, while patients wild-type for H3.3 show improved survival. Based on prognostic and therapeutic implications, our findings argue for H3.3-mutation testing at diagnosis, which should be rapidly integrated into the clinical decision-making algorithm, particularly in atypical DIPG.
Audience Academic
Author Buczkowicz, Pawel
Montpetit, Alexandre
Schwartzentruber, Jeremy
Fleming, Adam
Sturm, Dominik
Bouffet, Eric
Faury, Damien
Albrecht, Steffen
Korshunov, Andrey
Majewski, Jacek
Bartels, Ute
Bourret, Genevieve
Bourque, Guillaume
Hawkins, Cynthia
Pfister, Stefan M.
Bourgey, Mathieu
Liu, Xiao-Yang
Jones, David T.
Rakopoulos, Patricia
von Deimling, Andreas
Jabado, Nada
Letourneau, Louis
Kool, Marcel
Lichter, Peter
Khuong-Quang, Dong-Anh
Fontebasso, Adam M.
Lepage, Pierre
Author_xml – sequence: 1
  givenname: Dong-Anh
  surname: Khuong-Quang
  fullname: Khuong-Quang, Dong-Anh
  organization: Department of Human Genetics, McGill University
– sequence: 2
  givenname: Pawel
  surname: Buczkowicz
  fullname: Buczkowicz, Pawel
  organization: The Arthur and Sonia Labatt Brain Tumour Research Centre, The Hospital for Sick Children, Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto, Division of Pathology, The Hospital for Sick Children
– sequence: 3
  givenname: Patricia
  surname: Rakopoulos
  fullname: Rakopoulos, Patricia
  organization: The Arthur and Sonia Labatt Brain Tumour Research Centre, The Hospital for Sick Children, Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto
– sequence: 4
  givenname: Xiao-Yang
  surname: Liu
  fullname: Liu, Xiao-Yang
  organization: Department of Human Genetics, McGill University
– sequence: 5
  givenname: Adam M.
  surname: Fontebasso
  fullname: Fontebasso, Adam M.
  organization: Division of Experimental Medicine, McGill University
– sequence: 6
  givenname: Eric
  surname: Bouffet
  fullname: Bouffet, Eric
  organization: Division of Haematology–Oncology, The Hospital for Sick Children
– sequence: 7
  givenname: Ute
  surname: Bartels
  fullname: Bartels, Ute
  organization: Division of Haematology–Oncology, The Hospital for Sick Children
– sequence: 8
  givenname: Steffen
  surname: Albrecht
  fullname: Albrecht, Steffen
  organization: Department of Pathology, Montreal Children’s Hospital, McGill University Health Center
– sequence: 9
  givenname: Jeremy
  surname: Schwartzentruber
  fullname: Schwartzentruber, Jeremy
  organization: McGill University and Genome Quebec Innovation Center
– sequence: 10
  givenname: Louis
  surname: Letourneau
  fullname: Letourneau, Louis
  organization: McGill University and Genome Quebec Innovation Center
– sequence: 11
  givenname: Mathieu
  surname: Bourgey
  fullname: Bourgey, Mathieu
  organization: McGill University and Genome Quebec Innovation Center
– sequence: 12
  givenname: Guillaume
  surname: Bourque
  fullname: Bourque, Guillaume
  organization: McGill University and Genome Quebec Innovation Center
– sequence: 13
  givenname: Alexandre
  surname: Montpetit
  fullname: Montpetit, Alexandre
  organization: McGill University and Genome Quebec Innovation Center
– sequence: 14
  givenname: Genevieve
  surname: Bourret
  fullname: Bourret, Genevieve
  organization: McGill University and Genome Quebec Innovation Center
– sequence: 15
  givenname: Pierre
  surname: Lepage
  fullname: Lepage, Pierre
  organization: McGill University and Genome Quebec Innovation Center
– sequence: 16
  givenname: Adam
  surname: Fleming
  fullname: Fleming, Adam
  organization: Department of Paediatrics, Montreal Children’s Hospital, McGill University Health Center
– sequence: 17
  givenname: Peter
  surname: Lichter
  fullname: Lichter, Peter
  organization: Division of Molecular Genetics, The German Cancer Research Center (DKFZ)
– sequence: 18
  givenname: Marcel
  surname: Kool
  fullname: Kool, Marcel
  organization: Division of Pediatric Neuro-oncology, The German Cancer Research Center (DKFZ)
– sequence: 19
  givenname: Andreas
  surname: von Deimling
  fullname: von Deimling, Andreas
  organization: Clinical Cooperation Unit Neuropathology, The German Cancer Research Center (DKFZ)
– sequence: 20
  givenname: Dominik
  surname: Sturm
  fullname: Sturm, Dominik
  organization: Division of Pediatric Neuro-oncology, The German Cancer Research Center (DKFZ)
– sequence: 21
  givenname: Andrey
  surname: Korshunov
  fullname: Korshunov, Andrey
  organization: Clinical Cooperation Unit Neuropathology, The German Cancer Research Center (DKFZ)
– sequence: 22
  givenname: Damien
  surname: Faury
  fullname: Faury, Damien
  organization: Department of Paediatrics, Montreal Children’s Hospital, McGill University Health Center
– sequence: 23
  givenname: David T.
  surname: Jones
  fullname: Jones, David T.
  organization: Division of Pediatric Neuro-oncology, The German Cancer Research Center (DKFZ)
– sequence: 24
  givenname: Jacek
  surname: Majewski
  fullname: Majewski, Jacek
  organization: Department of Human Genetics, McGill University, McGill University and Genome Quebec Innovation Center
– sequence: 25
  givenname: Stefan M.
  surname: Pfister
  fullname: Pfister, Stefan M.
  organization: Division of Pediatric Neuro-oncology, The German Cancer Research Center (DKFZ), Department of Hematology and Oncology, Heidelberg University Hospital
– sequence: 26
  givenname: Nada
  surname: Jabado
  fullname: Jabado, Nada
  email: nada.jabado@mcgill.ca
  organization: Department of Human Genetics, McGill University, Division of Experimental Medicine, McGill University, Department of Paediatrics, Montreal Children’s Hospital, McGill University Health Center
– sequence: 27
  givenname: Cynthia
  surname: Hawkins
  fullname: Hawkins, Cynthia
  email: cynthia.hawkins@sickkids.ca
  organization: The Arthur and Sonia Labatt Brain Tumour Research Centre, The Hospital for Sick Children, Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto, Division of Pathology, The Hospital for Sick Children
BackLink https://www.ncbi.nlm.nih.gov/pubmed/22661320$$D View this record in MEDLINE/PubMed
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Issue 3
Keywords H3.3
DIPG
Targeted therapy
TP53
Survival
ATRX
Language English
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PublicationSubtitle Pathology and Mechanisms of Neurological Disease
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SSID ssj0012745
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Snippet Pediatric glioblastomas (GBM) including diffuse intrinsic pontine gliomas (DIPG) are devastating brain tumors with no effective therapy. Here, we investigated...
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proquest
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pubmed
crossref
springer
SourceType Open Access Repository
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Enrichment Source
Publisher
StartPage 439
SubjectTerms Adolescent
Algorithms
Biopsy
Brain cancer
Brain research
Brain stem
Brain Stem Neoplasms - genetics
Brain Stem Neoplasms - mortality
Brain Stem Neoplasms - pathology
Brain tumors
Cancer research
Cancer therapies
Child
Child, Preschool
Children
Clinical trials
Comparative analysis
copy number
Cortex
Decision making
Female
Gene Expression Profiling
Genetic aspects
Glioblastoma
Glioma
Glioma - genetics
Glioma - mortality
Glioma - pathology
Gliomas
Histones
Histones - genetics
Hospitals
Humans
Infant
Kinases
Male
Medical research
Medicine
Medicine & Public Health
Mutation
Myc protein
Neurosciences
Original Paper
p53 protein
Pathology
Pediatrics
Platelet-derived growth factor
Pons - pathology
Prognosis
Survival
Survival Rate
Tumor proteins
Tumors
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Title K27M mutation in histone H3.3 defines clinically and biologically distinct subgroups of pediatric diffuse intrinsic pontine gliomas
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Volume 124
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