author_facet Büschges, Rainer
Ichimura, Koichi
Weber, Ruthild G.
Reifenberger, Guido
Collins, V. Peter
Büschges, Rainer
Ichimura, Koichi
Weber, Ruthild G.
Reifenberger, Guido
Collins, V. Peter
author Büschges, Rainer
Ichimura, Koichi
Weber, Ruthild G.
Reifenberger, Guido
Collins, V. Peter
spellingShingle Büschges, Rainer
Ichimura, Koichi
Weber, Ruthild G.
Reifenberger, Guido
Collins, V. Peter
Brain Pathology
Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
Neurology (clinical)
Pathology and Forensic Medicine
General Neuroscience
author_sort büschges, rainer
spelling Büschges, Rainer Ichimura, Koichi Weber, Ruthild G. Reifenberger, Guido Collins, V. Peter 1015-6305 1750-3639 Wiley Neurology (clinical) Pathology and Forensic Medicine General Neuroscience http://dx.doi.org/10.1111/j.1750-3639.2002.tb00429.x <jats:p>Using comparative genomic hybridization (CGH) we have previously identified amplification at 17q21‐qter as a common aberration in anaplastic meningiomas but not in atypical or benign meningiomas (19). To define the amplified genomic region, we analyzed 44 meningeal tumors, including 7 benign meningiomas of World Health Organization (WHO) grade I, 19 atypical meningiomas (WHO grade II) and 18 anaplastic meningiomas (WHO grade III) at 46 chromosome 17 loci (including 42 17q loci). In line with the CGH data we found evidence of increased numbers of alleles on 17q. The incidence rose with malignancy grade, culminating at 61% (11 of 18 cases) in the anaplastic meningioma group. The majority of cases showing increased allele numbers had, on average, low‐level allelic gains (relative increase in allele dosage of 2‐ to 5‐fold). Amplification of alleles (defined here as an average relative increase in allele dosage of more than 5 times) was detected in 2 anaplastic meningiomas. The amplification patterns in these tumors defined a number of common regions of amplification/increased allele copy number, the best defined include one between <jats:italic>D17S790</jats:italic> and <jats:italic>D17S1607</jats:italic> and one between <jats:italic>D17S1160</jats:italic> and <jats:italic>PS6K.</jats:italic> Real‐time PCR analysis of the <jats:italic>PS6K</jats:italic> candidate gene revealed no high‐level amplification despite this affecting adjacent loci. Our findings are fundamental for the identification of the gene(s) in 17q22‐q23 that is (are) the target(s) for increased copy number in anaplastic meningiomas and possibly other tumor types.</jats:p> Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas Brain Pathology
doi_str_mv 10.1111/j.1750-3639.2002.tb00429.x
facet_avail Online
Free
finc_class_facet Medizin
format ElectronicArticle
fullrecord blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTExMS9qLjE3NTAtMzYzOS4yMDAyLnRiMDA0MjkueA
id ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTExMS9qLjE3NTAtMzYzOS4yMDAyLnRiMDA0MjkueA
institution DE-Zwi2
DE-D161
DE-Gla1
DE-Zi4
DE-15
DE-Pl11
DE-Rs1
DE-105
DE-14
DE-Ch1
DE-L229
DE-D275
DE-Bn3
DE-Brt1
imprint Wiley, 2002
imprint_str_mv Wiley, 2002
issn 1750-3639
1015-6305
issn_str_mv 1750-3639
1015-6305
language English
mega_collection Wiley (CrossRef)
match_str buschges2002allelicgainandamplificationonthelongarmofchromosome17inanaplasticmeningiomas
publishDateSort 2002
publisher Wiley
recordtype ai
record_format ai
series Brain Pathology
source_id 49
title Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
title_unstemmed Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
title_full Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
title_fullStr Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
title_full_unstemmed Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
title_short Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
title_sort allelic gain and amplification on the long arm of chromosome 17 in anaplastic meningiomas
topic Neurology (clinical)
Pathology and Forensic Medicine
General Neuroscience
url http://dx.doi.org/10.1111/j.1750-3639.2002.tb00429.x
publishDate 2002
physical 145-153
description <jats:p>Using comparative genomic hybridization (CGH) we have previously identified amplification at 17q21‐qter as a common aberration in anaplastic meningiomas but not in atypical or benign meningiomas (19). To define the amplified genomic region, we analyzed 44 meningeal tumors, including 7 benign meningiomas of World Health Organization (WHO) grade I, 19 atypical meningiomas (WHO grade II) and 18 anaplastic meningiomas (WHO grade III) at 46 chromosome 17 loci (including 42 17q loci). In line with the CGH data we found evidence of increased numbers of alleles on 17q. The incidence rose with malignancy grade, culminating at 61% (11 of 18 cases) in the anaplastic meningioma group. The majority of cases showing increased allele numbers had, on average, low‐level allelic gains (relative increase in allele dosage of 2‐ to 5‐fold). Amplification of alleles (defined here as an average relative increase in allele dosage of more than 5 times) was detected in 2 anaplastic meningiomas. The amplification patterns in these tumors defined a number of common regions of amplification/increased allele copy number, the best defined include one between <jats:italic>D17S790</jats:italic> and <jats:italic>D17S1607</jats:italic> and one between <jats:italic>D17S1160</jats:italic> and <jats:italic>PS6K.</jats:italic> Real‐time PCR analysis of the <jats:italic>PS6K</jats:italic> candidate gene revealed no high‐level amplification despite this affecting adjacent loci. Our findings are fundamental for the identification of the gene(s) in 17q22‐q23 that is (are) the target(s) for increased copy number in anaplastic meningiomas and possibly other tumor types.</jats:p>
container_issue 2
container_start_page 145
container_title Brain Pathology
container_volume 12
format_de105 Article, E-Article
format_de14 Article, E-Article
format_de15 Article, E-Article
format_de520 Article, E-Article
format_de540 Article, E-Article
format_dech1 Article, E-Article
format_ded117 Article, E-Article
format_degla1 E-Article
format_del152 Buch
format_del189 Article, E-Article
format_dezi4 Article
format_dezwi2 Article, E-Article
format_finc Article, E-Article
format_nrw Article, E-Article
_version_ 1792344969874243587
geogr_code not assigned
last_indexed 2024-03-01T17:16:03.432Z
geogr_code_person not assigned
openURL url_ver=Z39.88-2004&ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fvufind.svn.sourceforge.net%3Agenerator&rft.title=Allelic+Gain+and+Amplification+on+the+Long+Arm+of+Chromosome+17+in+Anaplastic+Meningiomas&rft.date=2002-04-01&genre=article&issn=1750-3639&volume=12&issue=2&spage=145&epage=153&pages=145-153&jtitle=Brain+Pathology&atitle=Allelic+Gain+and+Amplification+on+the+Long+Arm+of+Chromosome+17+in+Anaplastic+Meningiomas&aulast=Collins&aufirst=V.+Peter&rft_id=info%3Adoi%2F10.1111%2Fj.1750-3639.2002.tb00429.x&rft.language%5B0%5D=eng
SOLR
_version_ 1792344969874243587
author Büschges, Rainer, Ichimura, Koichi, Weber, Ruthild G., Reifenberger, Guido, Collins, V. Peter
author_facet Büschges, Rainer, Ichimura, Koichi, Weber, Ruthild G., Reifenberger, Guido, Collins, V. Peter, Büschges, Rainer, Ichimura, Koichi, Weber, Ruthild G., Reifenberger, Guido, Collins, V. Peter
author_sort büschges, rainer
container_issue 2
container_start_page 145
container_title Brain Pathology
container_volume 12
description <jats:p>Using comparative genomic hybridization (CGH) we have previously identified amplification at 17q21‐qter as a common aberration in anaplastic meningiomas but not in atypical or benign meningiomas (19). To define the amplified genomic region, we analyzed 44 meningeal tumors, including 7 benign meningiomas of World Health Organization (WHO) grade I, 19 atypical meningiomas (WHO grade II) and 18 anaplastic meningiomas (WHO grade III) at 46 chromosome 17 loci (including 42 17q loci). In line with the CGH data we found evidence of increased numbers of alleles on 17q. The incidence rose with malignancy grade, culminating at 61% (11 of 18 cases) in the anaplastic meningioma group. The majority of cases showing increased allele numbers had, on average, low‐level allelic gains (relative increase in allele dosage of 2‐ to 5‐fold). Amplification of alleles (defined here as an average relative increase in allele dosage of more than 5 times) was detected in 2 anaplastic meningiomas. The amplification patterns in these tumors defined a number of common regions of amplification/increased allele copy number, the best defined include one between <jats:italic>D17S790</jats:italic> and <jats:italic>D17S1607</jats:italic> and one between <jats:italic>D17S1160</jats:italic> and <jats:italic>PS6K.</jats:italic> Real‐time PCR analysis of the <jats:italic>PS6K</jats:italic> candidate gene revealed no high‐level amplification despite this affecting adjacent loci. Our findings are fundamental for the identification of the gene(s) in 17q22‐q23 that is (are) the target(s) for increased copy number in anaplastic meningiomas and possibly other tumor types.</jats:p>
doi_str_mv 10.1111/j.1750-3639.2002.tb00429.x
facet_avail Online, Free
finc_class_facet Medizin
format ElectronicArticle
format_de105 Article, E-Article
format_de14 Article, E-Article
format_de15 Article, E-Article
format_de520 Article, E-Article
format_de540 Article, E-Article
format_dech1 Article, E-Article
format_ded117 Article, E-Article
format_degla1 E-Article
format_del152 Buch
format_del189 Article, E-Article
format_dezi4 Article
format_dezwi2 Article, E-Article
format_finc Article, E-Article
format_nrw Article, E-Article
geogr_code not assigned
geogr_code_person not assigned
id ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTExMS9qLjE3NTAtMzYzOS4yMDAyLnRiMDA0MjkueA
imprint Wiley, 2002
imprint_str_mv Wiley, 2002
institution DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1
issn 1750-3639, 1015-6305
issn_str_mv 1750-3639, 1015-6305
language English
last_indexed 2024-03-01T17:16:03.432Z
match_str buschges2002allelicgainandamplificationonthelongarmofchromosome17inanaplasticmeningiomas
mega_collection Wiley (CrossRef)
physical 145-153
publishDate 2002
publishDateSort 2002
publisher Wiley
record_format ai
recordtype ai
series Brain Pathology
source_id 49
spelling Büschges, Rainer Ichimura, Koichi Weber, Ruthild G. Reifenberger, Guido Collins, V. Peter 1015-6305 1750-3639 Wiley Neurology (clinical) Pathology and Forensic Medicine General Neuroscience http://dx.doi.org/10.1111/j.1750-3639.2002.tb00429.x <jats:p>Using comparative genomic hybridization (CGH) we have previously identified amplification at 17q21‐qter as a common aberration in anaplastic meningiomas but not in atypical or benign meningiomas (19). To define the amplified genomic region, we analyzed 44 meningeal tumors, including 7 benign meningiomas of World Health Organization (WHO) grade I, 19 atypical meningiomas (WHO grade II) and 18 anaplastic meningiomas (WHO grade III) at 46 chromosome 17 loci (including 42 17q loci). In line with the CGH data we found evidence of increased numbers of alleles on 17q. The incidence rose with malignancy grade, culminating at 61% (11 of 18 cases) in the anaplastic meningioma group. The majority of cases showing increased allele numbers had, on average, low‐level allelic gains (relative increase in allele dosage of 2‐ to 5‐fold). Amplification of alleles (defined here as an average relative increase in allele dosage of more than 5 times) was detected in 2 anaplastic meningiomas. The amplification patterns in these tumors defined a number of common regions of amplification/increased allele copy number, the best defined include one between <jats:italic>D17S790</jats:italic> and <jats:italic>D17S1607</jats:italic> and one between <jats:italic>D17S1160</jats:italic> and <jats:italic>PS6K.</jats:italic> Real‐time PCR analysis of the <jats:italic>PS6K</jats:italic> candidate gene revealed no high‐level amplification despite this affecting adjacent loci. Our findings are fundamental for the identification of the gene(s) in 17q22‐q23 that is (are) the target(s) for increased copy number in anaplastic meningiomas and possibly other tumor types.</jats:p> Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas Brain Pathology
spellingShingle Büschges, Rainer, Ichimura, Koichi, Weber, Ruthild G., Reifenberger, Guido, Collins, V. Peter, Brain Pathology, Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas, Neurology (clinical), Pathology and Forensic Medicine, General Neuroscience
title Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
title_full Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
title_fullStr Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
title_full_unstemmed Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
title_short Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
title_sort allelic gain and amplification on the long arm of chromosome 17 in anaplastic meningiomas
title_unstemmed Allelic Gain and Amplification on the Long Arm of Chromosome 17 in Anaplastic Meningiomas
topic Neurology (clinical), Pathology and Forensic Medicine, General Neuroscience
url http://dx.doi.org/10.1111/j.1750-3639.2002.tb00429.x