Distribution of TERT promoter mutations in pediatric and adult tumors of the nervous system

Hot spot mutations in the promoter region of telomerase reverse transcriptase ( TERT ) have recently been described in several human tumor entities. These mutations result in an upregulation of the telomerase complex activity and thus constitute a relevant mechanism for immortalization of tumor cell...

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Published inActa neuropathologica Vol. 126; no. 6; pp. 907 - 915
Main Authors Koelsche, Christian, Sahm, Felix, Capper, David, Reuss, David, Sturm, Dominik, Jones, David T. W., Kool, Marcel, Northcott, Paul A., Wiestler, Benedikt, Böhmer, Katja, Meyer, Jochen, Mawrin, Christian, Hartmann, Christian, Mittelbronn, Michel, Platten, Michael, Brokinkel, Benjamin, Seiz, Marcel, Herold-Mende, Christel, Unterberg, Andreas, Schittenhelm, Jens, Weller, Michael, Pfister, Stefan, Wick, Wolfgang, Korshunov, Andrey, von Deimling, Andreas
Format Journal Article
LanguageEnglish
Published Berlin/Heidelberg Springer Berlin Heidelberg 01.12.2013
Springer
Springer Nature B.V
Subjects
Adolescent
Adult
Analysis
Brain cancer
Brain Neoplasms - genetics
Brain Neoplasms - pathology
Brain tumors
Cancer research
Cell division
Child
Cooperation
Female
Genetic aspects
Geriatrics
Glioma - genetics
Glioma - pathology
Gliomas
Humans
Immunology
Male
Medical research
Medicine
Medicine & Public Health
Middle Aged
Mutation
Nervous system
Neuropathology
Neurosciences
Original Paper
Pathology
Pediatrics
Promoter Regions, Genetic
Research centers
Telomerase
Telomerase - genetics
Tumors
Yeast
Germany
Brain tumor
Promoter
Medulloblastoma
Glioblastoma
Mutation
Pediatric
Astrocytoma
Meningioma
Oligodendroglioma
Online AccessGet full text
ISSN0001-6322
1432-0533
1432-0533
DOI10.1007/s00401-013-1195-5

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Abstract Hot spot mutations in the promoter region of telomerase reverse transcriptase ( TERT ) have recently been described in several human tumor entities. These mutations result in an upregulation of the telomerase complex activity and thus constitute a relevant mechanism for immortalization of tumor cells. Knowledge of the TERT promoter status in tumors is likely to be of interest for molecular classification and as a potential target for therapy. We, therefore, performed a systematic analysis of TERT promoter mutations in 1,515 tumors of the human nervous system and its coverings including 373 pediatric and 1,142 adult patients. We detected a total of 327 mutations. TERT promoter mutations were exceedingly rare in tumors typically encountered in pediatric patients. In entities typically encountered in adult patients TERT promoter mutations were strongly associated with older age ( p  < 0.0001). Highest mutation frequencies were detected in gliosarcomas (81 %), oligodendrogliomas (78 %), oligoastrocytomas (58 %), primary glioblastomas (54 %), and solitary fibrous tumors (50 %). Related to other molecular alterations, TERT promoter mutations were strongly associated with 1p/19q loss ( p  < 0.0001), but inversely associated with loss of ATRX expression ( p  < 0.0001) and IDH1/IDH2 mutations ( p  < 0.0001). TERT promoter mutations are typically found in adult patients and occur in a highly tumor type-associated distribution.
AbstractList Hot spot mutations in the promoter region of telomerase reverse transcriptase (TERT) have recently been described in several human tumor entities. These mutations result in an upregulation of the telomerase complex activity and thus constitute a relevant mechanism for immortalization of tumor cells. Knowledge of the TERT promoter status in tumors is likely to be of interest for molecular classification and as a potential target for therapy. We, therefore, performed a systematic analysis of TERT promoter mutations in 1,515 tumors of the human nervous system and its coverings including 373 pediatric and 1,142 adult patients. We detected a total of 327 mutations. TERT promoter mutations were exceedingly rare in tumors typically encountered in pediatric patients. In entities typically encountered in adult patients TERT promoter mutations were strongly associated with older age (p < 0.0001). Highest mutation frequencies were detected in gliosarcomas (81 %), oligodendrogliomas (78 %), oligoastrocytomas (58 %), primary glioblastomas (54 %), and solitary fibrous tumors (50 %). Related to other molecular alterations, TERT promoter mutations were strongly associated with 1p/19q loss (p < 0.0001), but inversely associated with loss of ATRX expression (p < 0.0001) and IDH1/IDH2 mutations (p < 0.0001). TERT promoter mutations are typically found in adult patients and occur in a highly tumor type-associated distribution.
Hot spot mutations in the promoter region of telomerase reverse transcriptase (TERT) have recently been described in several human tumor entities. These mutations result in an upregulation of the telomerase complex activity and thus constitute a relevant mechanism for immortalization of tumor cells. Knowledge of the TERT promoter status in tumors is likely to be of interest for molecular classification and as a potential target for therapy. We, therefore, performed a systematic analysis of TERT promoter mutations in 1,515 tumors of the human nervous system and its coverings including 373 pediatric and 1,142 adult patients. We detected a total of 327 mutations. TERT promoter mutations were exceedingly rare in tumors typically encountered in pediatric patients. In entities typically encountered in adult patients TERT promoter mutations were strongly associated with older age (p < 0.0001). Highest mutation frequencies were detected in gliosarcomas (81 %), oligodendrogliomas (78 %), oligoastrocytomas (58 %), primary glioblastomas (54 %), and solitary fibrous tumors (50 %). Related to other molecular alterations, TERT promoter mutations were strongly associated with 1p/19q loss (p < 0.0001), but inversely associated with loss of ATRX expression (p < 0.0001) and IDH1/IDH2 mutations (p < 0.0001). TERT promoter mutations are typically found in adult patients and occur in a highly tumor type-associated distribution.Hot spot mutations in the promoter region of telomerase reverse transcriptase (TERT) have recently been described in several human tumor entities. These mutations result in an upregulation of the telomerase complex activity and thus constitute a relevant mechanism for immortalization of tumor cells. Knowledge of the TERT promoter status in tumors is likely to be of interest for molecular classification and as a potential target for therapy. We, therefore, performed a systematic analysis of TERT promoter mutations in 1,515 tumors of the human nervous system and its coverings including 373 pediatric and 1,142 adult patients. We detected a total of 327 mutations. TERT promoter mutations were exceedingly rare in tumors typically encountered in pediatric patients. In entities typically encountered in adult patients TERT promoter mutations were strongly associated with older age (p < 0.0001). Highest mutation frequencies were detected in gliosarcomas (81 %), oligodendrogliomas (78 %), oligoastrocytomas (58 %), primary glioblastomas (54 %), and solitary fibrous tumors (50 %). Related to other molecular alterations, TERT promoter mutations were strongly associated with 1p/19q loss (p < 0.0001), but inversely associated with loss of ATRX expression (p < 0.0001) and IDH1/IDH2 mutations (p < 0.0001). TERT promoter mutations are typically found in adult patients and occur in a highly tumor type-associated distribution.
Hot spot mutations in the promoter region of telomerase reverse transcriptase ( TERT ) have recently been described in several human tumor entities. These mutations result in an upregulation of the telomerase complex activity and thus constitute a relevant mechanism for immortalization of tumor cells. Knowledge of the TERT promoter status in tumors is likely to be of interest for molecular classification and as a potential target for therapy. We, therefore, performed a systematic analysis of TERT promoter mutations in 1,515 tumors of the human nervous system and its coverings including 373 pediatric and 1,142 adult patients. We detected a total of 327 mutations. TERT promoter mutations were exceedingly rare in tumors typically encountered in pediatric patients. In entities typically encountered in adult patients TERT promoter mutations were strongly associated with older age ( p  < 0.0001). Highest mutation frequencies were detected in gliosarcomas (81 %), oligodendrogliomas (78 %), oligoastrocytomas (58 %), primary glioblastomas (54 %), and solitary fibrous tumors (50 %). Related to other molecular alterations, TERT promoter mutations were strongly associated with 1p/19q loss ( p  < 0.0001), but inversely associated with loss of ATRX expression ( p  < 0.0001) and IDH1/IDH2 mutations ( p  < 0.0001). TERT promoter mutations are typically found in adult patients and occur in a highly tumor type-associated distribution.
Hot spot mutations in the promoter region of telomerase reverse transcriptase (TERT) have recently been described in several human tumor entities. These mutations result in an upregulation of the telomerase complex activity and thus constitute a relevant mechanism for immortalization of tumor cells. Knowledge of the TERT promoter status in tumors is likely to be of interest for molecular classification and as a potential target for therapy. We, therefore, performed a systematic analysis of TERT promoter mutations in 1,515 tumors of the human nervous system and its coverings including 373 pediatric and 1,142 adult patients. We detected a total of 327 mutations. TERT promoter mutations were exceedingly rare in tumors typically encountered in pediatric patients. In entities typically encountered in adult patients TERT promoter mutations were strongly associated with older age (p < 0.0001). Highest mutation frequencies were detected in gliosarcomas (81%), oligodendrogliomas (78%), oligoastrocytomas (58%), primary glioblastomas (54%), and solitary fibrous tumors (50%). Related to other molecular alterations, TERT promoter mutations were strongly associated with 1p/19q loss (p < 0.0001), but inversely associated with loss of ATRX expression (p < 0.0001) and 1DH1/1DH2 mutations (p < 0.0001). TERT promoter mutations are typically found in adult patients and occur in a highly tumor type-associated distribution.
Hot spot mutations in the promoter region of telomerase reverse transcriptase (TERT) have recently been described in several human tumor entities. These mutations result in an upregulation of the telomerase complex activity and thus constitute a relevant mechanism for immortalization of tumor cells. Knowledge of the TERT promoter status in tumors is likely to be of interest for molecular classification and as a potential target for therapy. We, therefore, performed a systematic analysis of TERT promoter mutations in 1,515 tumors of the human nervous system and its coverings including 373 pediatric and 1,142 adult patients. We detected a total of 327 mutations. TERT promoter mutations were exceedingly rare in tumors typically encountered in pediatric patients. In entities typically encountered in adult patients TERT promoter mutations were strongly associated with older age (p < 0.0001). Highest mutation frequencies were detected in gliosarcomas (81 %), oligodendrogliomas (78 %), oligoastrocytomas (58 %), primary glioblastomas (54 %), and solitary fibrous tumors (50 %). Related to other molecular alterations, TERT promoter mutations were strongly associated with 1p/19q loss (p < 0.0001), but inversely associated with loss of ATRX expression (p < 0.0001) and IDH1/IDH2 mutations (p < 0.0001). TERT promoter mutations are typically found in adult patients and occur in a highly tumor type-associated distribution.[PUBLICATION ABSTRACT]
Hot spot mutations in the promoter region of telomerase reverse transcriptase (TERT) have recently been described in several human tumor entities. These mutations result in an upregulation of the telomerase complex activity and thus constitute a relevant mechanism for immortalization of tumor cells. Knowledge of the TERT promoter status in tumors is likely to be of interest for molecular classification and as a potential target for therapy. We, therefore, performed a systematic analysis of TERT promoter mutations in 1,515 tumors of the human nervous system and its coverings including 373 pediatric and 1,142 adult patients. We detected a total of 327 mutations. TERT promoter mutations were exceedingly rare in tumors typically encountered in pediatric patients. In entities typically encountered in adult patients TERT promoter mutations were strongly associated with older age (p < 0.0001). Highest mutation frequencies were detected in gliosarcomas (81%), oligodendrogliomas (78%), oligoastrocytomas (58%), primary glioblastomas (54%), and solitary fibrous tumors (50%). Related to other molecular alterations, TERT promoter mutations were strongly associated with 1p/19q loss (p < 0.0001), but inversely associated with loss of ATRX expression (p < 0.0001) and 1DH1/1DH2 mutations (p < 0.0001). TERT promoter mutations are typically found in adult patients and occur in a highly tumor type-associated distribution. Keywords Astrocytoma * Oligodendroglioma * Glioblastoma * Meningioma * Medulloblastoma * Brain tumor * Pediatric * TERT * Promoter * Mutation
Audience Academic
Author Meyer, Jochen
Sturm, Dominik
Brokinkel, Benjamin
Sahm, Felix
Reuss, David
Koelsche, Christian
Northcott, Paul A.
Wick, Wolfgang
Wiestler, Benedikt
Korshunov, Andrey
Seiz, Marcel
Mittelbronn, Michel
Pfister, Stefan
Schittenhelm, Jens
Jones, David T. W.
Platten, Michael
Weller, Michael
Unterberg, Andreas
Herold-Mende, Christel
Hartmann, Christian
von Deimling, Andreas
Böhmer, Katja
Kool, Marcel
Capper, David
Mawrin, Christian
Author_xml – sequence: 1
  givenname: Christian
  surname: Koelsche
  fullname: Koelsche, Christian
  organization: Department of Neuropathology, Institute of Pathology, Ruprecht-Karls-University Heidelberg, Clinical Cooperation Unit Neuropathology, German Cancer Research Center Heidelberg (DKFZ)
– sequence: 2
  givenname: Felix
  surname: Sahm
  fullname: Sahm, Felix
  organization: Department of Neuropathology, Institute of Pathology, Ruprecht-Karls-University Heidelberg, Clinical Cooperation Unit Neuropathology, German Cancer Research Center Heidelberg (DKFZ)
– sequence: 3
  givenname: David
  surname: Capper
  fullname: Capper, David
  organization: Department of Neuropathology, Institute of Pathology, Ruprecht-Karls-University Heidelberg, Clinical Cooperation Unit Neuropathology, German Cancer Research Center Heidelberg (DKFZ)
– sequence: 4
  givenname: David
  surname: Reuss
  fullname: Reuss, David
  organization: Department of Neuropathology, Institute of Pathology, Ruprecht-Karls-University Heidelberg, Clinical Cooperation Unit Neuropathology, German Cancer Research Center Heidelberg (DKFZ)
– sequence: 5
  givenname: Dominik
  surname: Sturm
  fullname: Sturm, Dominik
  organization: Department of Pediatric Oncology, Hematology and Immunology, Ruprecht-Karls-University Heidelberg, Division of Pediatric Neurooncology, German Cancer Research Center Heidelberg (DKFZ)
– sequence: 6
  givenname: David T. W.
  surname: Jones
  fullname: Jones, David T. W.
  organization: Division of Pediatric Neurooncology, German Cancer Research Center Heidelberg (DKFZ)
– sequence: 7
  givenname: Marcel
  surname: Kool
  fullname: Kool, Marcel
  organization: Division of Pediatric Neurooncology, German Cancer Research Center Heidelberg (DKFZ)
– sequence: 8
  givenname: Paul A.
  surname: Northcott
  fullname: Northcott, Paul A.
  organization: Division of Pediatric Neurooncology, German Cancer Research Center Heidelberg (DKFZ)
– sequence: 9
  givenname: Benedikt
  surname: Wiestler
  fullname: Wiestler, Benedikt
  organization: Department of Neurooncology, Neurology Clinic and National Center for Tumor Disease, University of Heidelberg and German Cancer Research Center, Clinical Cooperation Unit Neurooncology, German Cancer Research Center (DKFZ)
– sequence: 10
  givenname: Katja
  surname: Böhmer
  fullname: Böhmer, Katja
  organization: Department of Neuropathology, Institute of Pathology, Ruprecht-Karls-University Heidelberg
– sequence: 11
  givenname: Jochen
  surname: Meyer
  fullname: Meyer, Jochen
  organization: Clinical Cooperation Unit Neuropathology, German Cancer Research Center Heidelberg (DKFZ)
– sequence: 12
  givenname: Christian
  surname: Mawrin
  fullname: Mawrin, Christian
  organization: Department of Neuropathology, Otto von Guericke University Magdeburg
– sequence: 13
  givenname: Christian
  surname: Hartmann
  fullname: Hartmann, Christian
  organization: Department of Neuropathology, Institute of Pathology, Medizinische Hochschule Hannover
– sequence: 14
  givenname: Michel
  surname: Mittelbronn
  fullname: Mittelbronn, Michel
  organization: Neurological Institute (Edinger-Institute), Goethe University, German Cancer Consortium (DKTK) Heidelberg
– sequence: 15
  givenname: Michael
  surname: Platten
  fullname: Platten, Michael
  organization: Department of Neurooncology, Neurology Clinic and National Center for Tumor Disease, University of Heidelberg and German Cancer Research Center, Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Research Center (DKFZ)
– sequence: 16
  givenname: Benjamin
  surname: Brokinkel
  fullname: Brokinkel, Benjamin
  organization: Institute of Neuropathology, University Hospital Münster
– sequence: 17
  givenname: Marcel
  surname: Seiz
  fullname: Seiz, Marcel
  organization: Department of Neurosurgery, University Medical Center Mannheim, Medical Faculty Mannheim, Heidelberg University
– sequence: 18
  givenname: Christel
  surname: Herold-Mende
  fullname: Herold-Mende, Christel
  organization: Department of Neurosurgery, University Hospital Heidelberg
– sequence: 19
  givenname: Andreas
  surname: Unterberg
  fullname: Unterberg, Andreas
  organization: Department of Neurosurgery, University Hospital Heidelberg
– sequence: 20
  givenname: Jens
  surname: Schittenhelm
  fullname: Schittenhelm, Jens
  organization: Department of Neuropathology, Institute of Pathology and Neuropathology, University Tübingen
– sequence: 21
  givenname: Michael
  surname: Weller
  fullname: Weller, Michael
  organization: Department of Neurology, University Hospital Zurich and Center for Neurosciences, University of Zurich
– sequence: 22
  givenname: Stefan
  surname: Pfister
  fullname: Pfister, Stefan
  organization: Department of Pediatric Oncology, Hematology and Immunology, Ruprecht-Karls-University Heidelberg, Division of Pediatric Neurooncology, German Cancer Research Center Heidelberg (DKFZ)
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  givenname: Wolfgang
  surname: Wick
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  organization: Department of Neurooncology, Neurology Clinic and National Center for Tumor Disease, University of Heidelberg and German Cancer Research Center, Clinical Cooperation Unit Neurooncology, German Cancer Research Center (DKFZ)
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  givenname: Andrey
  surname: Korshunov
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  organization: Department of Neuropathology, Institute of Pathology, Ruprecht-Karls-University Heidelberg, Clinical Cooperation Unit Neuropathology, German Cancer Research Center Heidelberg (DKFZ)
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  givenname: Andreas
  surname: von Deimling
  fullname: von Deimling, Andreas
  email: andreas.vondeimling@med.uni-heidelberg.de
  organization: Department of Neuropathology, Institute of Pathology, Ruprecht-Karls-University Heidelberg, Clinical Cooperation Unit Neuropathology, German Cancer Research Center Heidelberg (DKFZ)
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24154961$$D View this record in MEDLINE/PubMed
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Issue 6
Keywords Brain tumor
Promoter
Medulloblastoma
Glioblastoma
Mutation
Pediatric
Astrocytoma
Meningioma
Oligodendroglioma
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PublicationSubtitle Pathology and Mechanisms of Neurological Disease
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Snippet Hot spot mutations in the promoter region of telomerase reverse transcriptase ( TERT ) have recently been described in several human tumor entities. These...
Hot spot mutations in the promoter region of telomerase reverse transcriptase (TERT) have recently been described in several human tumor entities. These...
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SubjectTerms Adolescent
Adult
Analysis
Brain cancer
Brain Neoplasms - genetics
Brain Neoplasms - pathology
Brain tumors
Cancer research
Cell division
Child
Cooperation
Female
Genetic aspects
Geriatrics
Glioma - genetics
Glioma - pathology
Gliomas
Humans
Immunology
Male
Medical research
Medicine
Medicine & Public Health
Middle Aged
Mutation
Nervous system
Neuropathology
Neurosciences
Original Paper
Pathology
Pediatrics
Promoter Regions, Genetic
Research centers
Telomerase
Telomerase - genetics
Tumors
Yeast
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Title Distribution of TERT promoter mutations in pediatric and adult tumors of the nervous system
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