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 in | Nature genetics Vol. 41; no. 4; pp. 465 - 472 |
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Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
Nature Publishing Group US
01.04.2009
Nature Publishing Group |
Subjects | |
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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. |
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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 – name: 9 Department of Pathology, Johns Hopkins University, Baltimore, Maryland, USA – name: 19 Department of Pathology, Duke University, Durham, North Carolina, USA – name: 2 Program in Developmental and Stem Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada – 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 fullname: Gillespie, Yancey organization: Department of Surgery, University of Alabama – givenname: Stephen W surname: Scherer fullname: Scherer, Stephen W organization: The Centre for Applied Genomics, The Hospital for Sick Children Department of Molecular Genetics, University of Toronto – givenname: Richard J surname: Gilbertson fullname: Gilbertson, Richard J organization: Department of Developmental Neurobiology, St Jude Children's Research Hospital Department of Oncology, St Jude Children's Research Hospital – givenname: David W surname: Ellison fullname: Ellison, David W organization: Department of Pathology, St Jude Children's Research Hospital – givenname: Boleslaw surname: Lach fullname: Lach, Boleslaw organization: Department of Pathology and Molecular Medicine, McMaster University – givenname: Carlos G surname: Carlotti fullname: Carlotti, Carlos G organization: Division of Neurosurgery, Department of Surgery, Ribeirão Preto Medical School, University of São Paulo – givenname: Michael D surname: Taylor fullname: Taylor, Michael D 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 – givenname: J surname: Sunil Rao fullname: Sunil Rao, J organization: Department of Epidemiology and Biostatistics, Case Western Reserve University School of Medicine – givenname: Paul N surname: Kongkham fullname: Kongkham, Paul N organization: Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre Department of Laboratory Medicine & Pathobiology, University of Toronto – givenname: Adrian surname: Dubuc fullname: Dubuc, Adrian 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 – givenname: Ronald L surname: Hamilton fullname: Hamilton, Ronald L organization: Department of Pathology, Children's Hospital of Pittsburgh, University of Pittsburgh – givenname: Charles G surname: Eberhart fullname: Eberhart, Charles G organization: Department of Pathology, Johns Hopkins University – givenname: James T surname: Rutka fullname: Rutka, James T organization: Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre Department of Laboratory Medicine & Pathobiology, University of Toronto – givenname: Yukiko surname: Nakahara fullname: Nakahara, Yukiko organization: Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre Program in Developmental and Stem Cell Biology, The Hospital for Sick Children – givenname: Frederick surname: Boop fullname: Boop, Frederick organization: Division of Pediatric Neurosurgery, St. Jude Children's Research Hospital – givenname: Ian F surname: Pollack fullname: Pollack, Ian F organization: Department of Neurosurgery, Children's Hospital of Pittsburgh, University of Pittsburgh – givenname: Stephen surname: Mack fullname: Mack, Stephen 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 – givenname: Paul A surname: Northcott fullname: Northcott, Paul A 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 – givenname: Sid surname: Croul fullname: Croul, Sid organization: Department of Pathology, University Health Network, University of Toronto – givenname: Young-Shin surname: Ra fullname: Ra, Young-Shin organization: Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre – givenname: Timothy surname: Van Meter fullname: Van Meter, Timothy organization: Department of Neurosurgery, Medical College of Virginia – givenname: Jessica surname: Mcleod fullname: Mcleod, Jessica organization: Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre Program in Developmental and Stem Cell Biology, The Hospital for Sick Children – givenname: Richard surname: Grundy fullname: Grundy, Richard organization: University of Nottingham – givenname: Lars surname: Feuk fullname: Feuk, Lars organization: The Centre for Applied Genomics, The Hospital for Sick Children Department of Molecular Genetics, University of Toronto – givenname: Karen surname: Zilberberg fullname: Zilberberg, Karen 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 – givenname: Darrell surname: Bigner fullname: Bigner, Darrell organization: Department of Pathology, Duke University – givenname: John surname: Peacock fullname: Peacock, John organization: Division of Neurosurgery, Arthur and Sonia Labatt Brain Tumour Research Centre Program in Developmental and Stem Cell Biology, The Hospital for Sick Children – givenname: Wiesia surname: Grajkowska fullname: Grajkowska, Wiesia organization: Department of Pathology, Children's Memorial Health Institute – givenname: Xiaochong surname: Wu fullname: Wu, Xiaochong 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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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 |
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