Multiple recurrent genetic events converge on control of histone lysine methylation in medulloblastoma

We used high-resolution SNP genotyping to identify regions of genomic gain and loss in the genomes of 212 medulloblastomas, malignant pediatric brain tumors. We found focal amplifications of 15 known oncogenes and focal deletions of 20 known tumor suppressor genes (TSG), most not previously implicat...

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Published inNature genetics Vol. 41; no. 4; pp. 465 - 472
Main Authors Gillespie, Yancey, Scherer, Stephen W, Gilbertson, Richard J, Ellison, David W, Lach, Boleslaw, Carlotti, Carlos G, Taylor, Michael D, Sunil Rao, J, Kongkham, Paul N, Dubuc, Adrian, Hamilton, Ronald L, Eberhart, Charles G, Rutka, James T, Nakahara, Yukiko, Boop, Frederick, Pollack, Ian F, Mack, Stephen, Northcott, Paul A, Croul, Sid, Ra, Young-Shin, Van Meter, Timothy, Mcleod, Jessica, Grundy, Richard, Feuk, Lars, Zilberberg, Karen, Bigner, Darrell, Peacock, John, Grajkowska, Wiesia, Wu, Xiaochong
Format Journal Article
LanguageEnglish
Published New York Nature Publishing Group US 01.04.2009
Nature Publishing Group
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Abstract We used high-resolution SNP genotyping to identify regions of genomic gain and loss in the genomes of 212 medulloblastomas, malignant pediatric brain tumors. We found focal amplifications of 15 known oncogenes and focal deletions of 20 known tumor suppressor genes (TSG), most not previously implicated in medulloblastoma. Notably, we identified previously unknown amplifications and homozygous deletions, including recurrent, mutually exclusive, highly focal genetic events in genes targeting histone lysine methylation, particularly that of histone 3, lysine 9 (H3K9). Post-translational modification of histone proteins is critical for regulation of gene expression, can participate in determination of stem cell fates and has been implicated in carcinogenesis. Consistent with our genetic data, restoration of expression of genes controlling H3K9 methylation greatly diminishes proliferation of medulloblastoma in vitro. Copy number aberrations of genes with critical roles in writing, reading, removing and blocking the state of histone lysine methylation, particularly at H3K9, suggest that defective control of the histone code contributes to the pathogenesis of medulloblastoma.
AbstractList We used high-resolution SNP genotyping to identify regions of genomic gain and loss in the genomes of 212 medulloblastomas, malignant pediatric brain tumors. We found focal amplifications of 15 known oncogenes and focal deletions of 20 known tumor suppressor genes (TSG), most not previously implicated in medulloblastoma. Notably, we identified previously unknown amplifications and homozygous deletions, including recurrent, mutually exclusive, highly focal genetic events in genes targeting histone lysine methylation, particularly that of histone 3, lysine 9 (H3K9). Post- translational modification of histone proteins is critical for regulation of gene expression, can participate in determination of stem cell fates and has been implicated in carcinogenesis. Consistent with our genetic data, restoration of expression of genes controlling H3K9 methylation greatly diminishes proliferation of medulloblastoma in vitro. Copy number aberrations of genes with critical roles in writing, reading, removing and blocking the state of histone lysine methylation, particularly at H3K9, suggest that defective control of the histone code contributes to the pathogenesis of medulloblastoma.
We used high-resolution SNP genotyping to identify regions of genomic gain and loss in the genomes of 212 medulloblastomas, malignant pediatric brain tumors. We found focal amplifications of 15 known oncogenes and focal deletions of 20 known tumor suppressor genes (TSG), most not previously implicated in medulloblastoma. Notably, we identified previously unknown amplifications and homozygous deletions, including recurrent, mutually exclusive, highly focal genetic events in genes targeting histone lysine methylation, particularly that of histone 3, lysine 9 (H3K9). Post-translational modification of histone proteins is critical for regulation of gene expression, can participate in determination of stem cell fates and has been implicated in carcinogenesis. Consistent with our genetic data, restoration of expression of genes controlling H3K9 methylation greatly diminishes proliferation of medulloblastoma in vitro. Copy number aberrations of genes with critical roles in writing, reading, removing and blocking the state of histone lysine methylation, particularly at H3K9, suggest that defective control of the histone code contributes to the pathogenesis of medulloblastoma. [PUBLICATION ABSTRACT]
We used high-resolution SNP genotyping to identify regions of genomic gain and loss in the genomes of 212 medulloblastomas, malignant pediatric brain tumors. We found focal amplifications of 15 known oncogenes and focal deletions of 20 known tumor suppressor genes (TSG), most not previously implicated in medulloblastoma. Notably, we identified previously unknown amplifications and homozygous deletions, including recurrent, mutually exclusive, highly focal genetic events in genes targeting histone lysine methylation, particularly that of histone 3, lysine 9 (H3K9). Post-translational modification of histone proteins is critical for regulation of gene expression, can participate in determination of stem cell fates and has been implicated in carcinogenesis. Consistent with our genetic data, restoration of expression of genes controlling H3K9 methylation greatly diminishes proliferation of medulloblastoma in vitro . Copy number aberrations of genes with critical roles in writing, reading, removing and blocking the state of histone lysine methylation, particularly at H3K9, suggest that defective control of the histone code contributes to the pathogenesis of medulloblastoma.
We used high-resolution SNP genotyping to identify regions of genomic gain and loss in the genomes of 212 medulloblastomas, malignant pediatric brain tumors. We found focal amplifications of 15 known oncogenes and focal deletions of 20 known tumor suppressor genes (TSG), most not previously implicated in medulloblastoma. Notably, we identified previously unknown amplifications and homozygous deletions, including recurrent, mutually exclusive, highly focal genetic events in genes targeting histone lysine methylation, particularly that of histone 3, lysine 9 (H3K9). Post-translational modification of histone proteins is critical for regulation of gene expression, can participate in determination of stem cell fates and has been implicated in carcinogenesis. Consistent with our genetic data, restoration of expression of genes controlling H3K9 methylation greatly diminishes proliferation of medulloblastoma in vitro. Copy number aberrations of genes I with critical roles in writing, reading, removing and blocking the state of histone lysine methylation, particularly at H3K9, suggest that defective control of the histone code contributes to the pathogenesis of medulloblastoma.
Michael Taylor and colleagues identify copy number aberrations of genes with critical roles in writing, reading, removing and blocking the state of histone lysine methylation, indicating that defective control of the histone code contributes to the pathogenesis of medulloblastoma. We used high-resolution SNP genotyping to identify regions of genomic gain and loss in the genomes of 212 medulloblastomas, malignant pediatric brain tumors. We found focal amplifications of 15 known oncogenes and focal deletions of 20 known tumor suppressor genes (TSG), most not previously implicated in medulloblastoma. Notably, we identified previously unknown amplifications and homozygous deletions, including recurrent, mutually exclusive, highly focal genetic events in genes targeting histone lysine methylation, particularly that of histone 3, lysine 9 (H3K9). Post-translational modification of histone proteins is critical for regulation of gene expression, can participate in determination of stem cell fates and has been implicated in carcinogenesis. Consistent with our genetic data, restoration of expression of genes controlling H3K9 methylation greatly diminishes proliferation of medulloblastoma in vitro . Copy number aberrations of genes with critical roles in writing, reading, removing and blocking the state of histone lysine methylation, particularly at H3K9, suggest that defective control of the histone code contributes to the pathogenesis of medulloblastoma.
Audience Academic
Author Gillespie, Yancey
Feuk, Lars
Mack, Stephen
Pollack, Ian F
Van Meter, Timothy
Bigner, Darrell
Peacock, John
Grundy, Richard
Dubuc, Adrian
Croul, Sid
Eberhart, Charles G
Lach, Boleslaw
Hamilton, Ronald L
Kongkham, Paul N
Mcleod, Jessica
Zilberberg, Karen
Nakahara, Yukiko
Grajkowska, Wiesia
Carlotti, Carlos G
Scherer, Stephen W
Gilbertson, Richard J
Northcott, Paul A
Ra, Young-Shin
Boop, Frederick
Wu, Xiaochong
Ellison, David W
Sunil Rao, J
Taylor, Michael D
Rutka, James T
AuthorAffiliation 14 Department of Neurosurgery, Children’s Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
20 Departments of Developmental Neurobiology, St Jude Children’s Research Hospital, Memphis, Tennessee, USA
17 Division of Neurosurgery, Department of Surgery, Ribeirão Preto Medical School, University of São Paulo, São Paulo, Brazil
9 Department of Pathology, Johns Hopkins University, Baltimore, Maryland, USA
18 Division of Pediatric Neurosurgery, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA
11 Department of Surgery, University of Alabama, Birmingham, Alabama, USA
12 Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
19 Department of Pathology, Duke University, Durham, North Carolina, USA
3 Department of Laboratory Medicine & Pathobiology, University of Toronto, Toronto, Ontario, Canada
7 Department of Pathology, University Health Network, University of Toronto, Toronto, Ontario, Canada
1 Division of Neurosurgery,
AuthorAffiliation_xml – name: 4 The Centre for Applied Genomics, The Hospital for Sick Children, Toronto, Ontario, Canada
– name: 14 Department of Neurosurgery, Children’s Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
– name: 6 Department of Pathology, St Jude Children’s Research Hospital, Memphis, Tennessee, USA
– name: 8 Department of Epidemiology and Biostatistics, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA
– name: 20 Departments of Developmental Neurobiology, St Jude Children’s Research Hospital, Memphis, Tennessee, USA
– name: 21 Departments of Oncology, St Jude Children’s Research Hospital, Memphis, Tennessee, USA
– name: 12 Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
– name: 15 Department of Pathology, Children’s Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
– name: 17 Division of Neurosurgery, Department of Surgery, Ribeirão Preto Medical School, University of São Paulo, São Paulo, Brazil
– name: 16 Department of Neurosurgery, Medical College of Virginia, Richmond, Virginia, USA
– name: 10 Department of Pathology, Children’s Memorial Health Institute, Warsaw, Poland
– name: 1 Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre, The Hospital for Sick Children, Toronto, Ontario, Canada
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– name: 19 Department of Pathology, Duke University, Durham, North Carolina, USA
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– name: 7 Department of Pathology, University Health Network, University of Toronto, Toronto, Ontario, Canada
– name: 13 University of Nottingham, Nottingham, UK
– name: 5 Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada
– name: 11 Department of Surgery, University of Alabama, Birmingham, Alabama, USA
– name: 3 Department of Laboratory Medicine & Pathobiology, University of Toronto, Toronto, Ontario, Canada
– name: 18 Division of Pediatric Neurosurgery, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA
Author_xml – givenname: Yancey
  surname: Gillespie
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  organization: Department of Surgery, University of Alabama
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  organization: Department of Epidemiology and Biostatistics, Case Western Reserve University School of Medicine
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  organization: Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre Program in Developmental and Stem Cell Biology, The Hospital for Sick Children Department of Laboratory Medicine & Pathobiology, University of Toronto
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  surname: Hamilton
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  organization: Department of Pathology, Children's Hospital of Pittsburgh, University of Pittsburgh
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  surname: Northcott
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  surname: Croul
  fullname: Croul, Sid
  organization: Department of Pathology, University Health Network, University of Toronto
– givenname: Young-Shin
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  organization: Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre
– givenname: Timothy
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  organization: Department of Neurosurgery, Medical College of Virginia
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  surname: Mcleod
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  organization: Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre Program in Developmental and Stem Cell Biology, The Hospital for Sick Children
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  organization: Department of Pathology, Duke University
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  organization: Department of Pathology, Children's Memorial Health Institute
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  organization: Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre Program in Developmental and Stem Cell Biology, The Hospital for Sick Children
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21344272$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/19270706$$D View this record in MEDLINE/PubMed
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Keywords Nervous system diseases
Regulation(control)
Lysine
Medulloblastoma
Central nervous system disease
Genetics
Malignant tumor
Recurrent
Histone
Methylation
Cancer
Cerebral disorder
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Snippet We used high-resolution SNP genotyping to identify regions of genomic gain and loss in the genomes of 212 medulloblastomas, malignant pediatric brain tumors....
Michael Taylor and colleagues identify copy number aberrations of genes with critical roles in writing, reading, removing and blocking the state of histone...
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SubjectTerms Agriculture
Animal Genetics and Genomics
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
Brain
Brain cancer
Brain tumors
Cancer Research
Carcinogenesis
Cerebellar Neoplasms - enzymology
Cerebellar Neoplasms - genetics
Chromosomes
DNA damage
Fundamental and applied biological sciences. Psychology
Gene Amplification
Gene Deletion
Gene Function
Genes
Genes, Tumor Suppressor
Genetic aspects
Genetics
Genetics of eukaryotes. Biological and molecular evolution
Genome, Human
Histone-Lysine N-Methyltransferase - genetics
Histones - metabolism
Human Genetics
Humans
letter
Lysine - metabolism
Medical research
Medical sciences
Medulloblastoma
Medulloblastoma - enzymology
Medulloblastoma - genetics
Methylation
Neurology
Physiological aspects
Polymorphism, Single Nucleotide
Protein Processing, Post-Translational - genetics
Proteins
Risk factors
Sequence Deletion
Single nucleotide polymorphisms
Stem cells
Tumors of the nervous system. Phacomatoses
Title Multiple recurrent genetic events converge on control of histone lysine methylation in medulloblastoma
URI http://dx.doi.org/10.1038/ng.336
https://link.springer.com/article/10.1038/ng.336
https://www.ncbi.nlm.nih.gov/pubmed/19270706
https://www.proquest.com/docview/222637409
https://search.proquest.com/docview/20490830
https://pubmed.ncbi.nlm.nih.gov/PMC4454371
Volume 41
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