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Supratentorial primitive neuroectodermal tumors of the central nervous system frequently harbor deletions of the CDKN2A locus and other genomic aberrations distinct from medulloblastomas

Standard

Supratentorial primitive neuroectodermal tumors of the central nervous system frequently harbor deletions of the CDKN2A locus and other genomic aberrations distinct from medulloblastomas. / Pfister, Stefan; Remke, Marc; Toedt, Grischa; Werft, Wiebke; Benner, Axel; Mendrzyk, Frank; Wittmann, Andrea; Devens, Frauke; von Hoff, Katja; Rutkowski, Stefan; Kulozik, Andreas; Radlwimmer, Bernhard; Scheurlen, Wolfram; Lichter, Peter; Korshunov, Andrey.

in: GENE CHROMOSOME CANC, Jahrgang 46, Nr. 9, 09.2007, S. 839-51.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Pfister, S, Remke, M, Toedt, G, Werft, W, Benner, A, Mendrzyk, F, Wittmann, A, Devens, F, von Hoff, K, Rutkowski, S, Kulozik, A, Radlwimmer, B, Scheurlen, W, Lichter, P & Korshunov, A 2007, 'Supratentorial primitive neuroectodermal tumors of the central nervous system frequently harbor deletions of the CDKN2A locus and other genomic aberrations distinct from medulloblastomas', GENE CHROMOSOME CANC, Jg. 46, Nr. 9, S. 839-51. https://doi.org/10.1002/gcc.20471

APA

Pfister, S., Remke, M., Toedt, G., Werft, W., Benner, A., Mendrzyk, F., Wittmann, A., Devens, F., von Hoff, K., Rutkowski, S., Kulozik, A., Radlwimmer, B., Scheurlen, W., Lichter, P., & Korshunov, A. (2007). Supratentorial primitive neuroectodermal tumors of the central nervous system frequently harbor deletions of the CDKN2A locus and other genomic aberrations distinct from medulloblastomas. GENE CHROMOSOME CANC, 46(9), 839-51. https://doi.org/10.1002/gcc.20471

Vancouver

Pfister S, Remke M, Toedt G, Werft W, Benner A, Mendrzyk F et al. Supratentorial primitive neuroectodermal tumors of the central nervous system frequently harbor deletions of the CDKN2A locus and other genomic aberrations distinct from medulloblastomas. GENE CHROMOSOME CANC. 2007 Sep;46(9):839-51. https://doi.org/10.1002/gcc.20471

Bibtex

@article{a4a46eab61a74223af75e68375e3d2f3,
title = "Supratentorial primitive neuroectodermal tumors of the central nervous system frequently harbor deletions of the CDKN2A locus and other genomic aberrations distinct from medulloblastomas",
abstract = "Supratentorial primitive neuroectodermal tumors (stPNETs) and medulloblastomas have long been thought to arise from a common cell type in the subventricular germinal matrix. Because of the infrequent occurrence of stPNETs, little is known about their genetic background. Here, we performed a genome-wide screening for DNA copy-number aberrations in 10 supratentorial PNETs using array-based comparative genomic hybridization (array-CGH). Comparing our findings with data from a previous array-CGH study on 47 medulloblastomas, we identified differences in the frequency of copy-number losses at chromosome regions 1p12-22.1 and 9p, and gains at 19p, all of them more frequently occurring in stPNETs. In contrast to previous reports, we detected chromosome 17 aberrations by array-CGH in 2/10 stPNETs. To validate our findings obtained by array-CGH, we analyzed the loci of interest by fluorescence in situ hybridization in an independent set of 11 stPNETs and found deletions of 9p21 in 5/11 tumors of the second set, three of them being homozygous. All 9p21 deletions were associated with loss of CDKN2A protein expression. Altogether, CDKN2A deletions were detected in 7/21 stPNETs including four homozygous deletions, whereas such deletions were only found in 4/112 medulloblastomas, all of these being heterozygous (P < 0.001). Gains of 19p (14% vs. 0% in medulloblastomas, P = 0.02) were found to be significantly more frequent in stPNETs, whereas gains of 17q (14% vs. 45% in medulloblastomas, P = 0.02) were confirmed to be more frequent in medulloblastomas. These data further support the hypothesis of two different tumor entities of embryonal neuroepithelial tumors with characteristic genetic aberrations. (c) 2007 Wiley-Liss, Inc.",
keywords = "Cerebellar Neoplasms, Chromosome Deletion, Cyclin-Dependent Kinase Inhibitor p16, Gene Dosage, Genome, Human, Humans, In Situ Hybridization, Fluorescence, Medulloblastoma, Neuroectodermal Tumors, Primitive, Supratentorial Neoplasms",
author = "Stefan Pfister and Marc Remke and Grischa Toedt and Wiebke Werft and Axel Benner and Frank Mendrzyk and Andrea Wittmann and Frauke Devens and {von Hoff}, Katja and Stefan Rutkowski and Andreas Kulozik and Bernhard Radlwimmer and Wolfram Scheurlen and Peter Lichter and Andrey Korshunov",
year = "2007",
month = sep,
doi = "10.1002/gcc.20471",
language = "English",
volume = "46",
pages = "839--51",
journal = "GENE CHROMOSOME CANC",
issn = "1045-2257",
publisher = "Wiley-Liss Inc.",
number = "9",

}

RIS

TY - JOUR

T1 - Supratentorial primitive neuroectodermal tumors of the central nervous system frequently harbor deletions of the CDKN2A locus and other genomic aberrations distinct from medulloblastomas

AU - Pfister, Stefan

AU - Remke, Marc

AU - Toedt, Grischa

AU - Werft, Wiebke

AU - Benner, Axel

AU - Mendrzyk, Frank

AU - Wittmann, Andrea

AU - Devens, Frauke

AU - von Hoff, Katja

AU - Rutkowski, Stefan

AU - Kulozik, Andreas

AU - Radlwimmer, Bernhard

AU - Scheurlen, Wolfram

AU - Lichter, Peter

AU - Korshunov, Andrey

PY - 2007/9

Y1 - 2007/9

N2 - Supratentorial primitive neuroectodermal tumors (stPNETs) and medulloblastomas have long been thought to arise from a common cell type in the subventricular germinal matrix. Because of the infrequent occurrence of stPNETs, little is known about their genetic background. Here, we performed a genome-wide screening for DNA copy-number aberrations in 10 supratentorial PNETs using array-based comparative genomic hybridization (array-CGH). Comparing our findings with data from a previous array-CGH study on 47 medulloblastomas, we identified differences in the frequency of copy-number losses at chromosome regions 1p12-22.1 and 9p, and gains at 19p, all of them more frequently occurring in stPNETs. In contrast to previous reports, we detected chromosome 17 aberrations by array-CGH in 2/10 stPNETs. To validate our findings obtained by array-CGH, we analyzed the loci of interest by fluorescence in situ hybridization in an independent set of 11 stPNETs and found deletions of 9p21 in 5/11 tumors of the second set, three of them being homozygous. All 9p21 deletions were associated with loss of CDKN2A protein expression. Altogether, CDKN2A deletions were detected in 7/21 stPNETs including four homozygous deletions, whereas such deletions were only found in 4/112 medulloblastomas, all of these being heterozygous (P < 0.001). Gains of 19p (14% vs. 0% in medulloblastomas, P = 0.02) were found to be significantly more frequent in stPNETs, whereas gains of 17q (14% vs. 45% in medulloblastomas, P = 0.02) were confirmed to be more frequent in medulloblastomas. These data further support the hypothesis of two different tumor entities of embryonal neuroepithelial tumors with characteristic genetic aberrations. (c) 2007 Wiley-Liss, Inc.

AB - Supratentorial primitive neuroectodermal tumors (stPNETs) and medulloblastomas have long been thought to arise from a common cell type in the subventricular germinal matrix. Because of the infrequent occurrence of stPNETs, little is known about their genetic background. Here, we performed a genome-wide screening for DNA copy-number aberrations in 10 supratentorial PNETs using array-based comparative genomic hybridization (array-CGH). Comparing our findings with data from a previous array-CGH study on 47 medulloblastomas, we identified differences in the frequency of copy-number losses at chromosome regions 1p12-22.1 and 9p, and gains at 19p, all of them more frequently occurring in stPNETs. In contrast to previous reports, we detected chromosome 17 aberrations by array-CGH in 2/10 stPNETs. To validate our findings obtained by array-CGH, we analyzed the loci of interest by fluorescence in situ hybridization in an independent set of 11 stPNETs and found deletions of 9p21 in 5/11 tumors of the second set, three of them being homozygous. All 9p21 deletions were associated with loss of CDKN2A protein expression. Altogether, CDKN2A deletions were detected in 7/21 stPNETs including four homozygous deletions, whereas such deletions were only found in 4/112 medulloblastomas, all of these being heterozygous (P < 0.001). Gains of 19p (14% vs. 0% in medulloblastomas, P = 0.02) were found to be significantly more frequent in stPNETs, whereas gains of 17q (14% vs. 45% in medulloblastomas, P = 0.02) were confirmed to be more frequent in medulloblastomas. These data further support the hypothesis of two different tumor entities of embryonal neuroepithelial tumors with characteristic genetic aberrations. (c) 2007 Wiley-Liss, Inc.

KW - Cerebellar Neoplasms

KW - Chromosome Deletion

KW - Cyclin-Dependent Kinase Inhibitor p16

KW - Gene Dosage

KW - Genome, Human

KW - Humans

KW - In Situ Hybridization, Fluorescence

KW - Medulloblastoma

KW - Neuroectodermal Tumors, Primitive

KW - Supratentorial Neoplasms

U2 - 10.1002/gcc.20471

DO - 10.1002/gcc.20471

M3 - SCORING: Journal article

C2 - 17592618

VL - 46

SP - 839

EP - 851

JO - GENE CHROMOSOME CANC

JF - GENE CHROMOSOME CANC

SN - 1045-2257

IS - 9

ER -