Infrequency of p53 gene mutations in ependymomas

Ependymomas, which comprise 5% of central nervous system tumors, have not been extensively characterized genetically. The p53 tumor suppressor gene is frequently mutated in human cancer, and is important in the pathogenesis of other central nervous system (CNS) tumors. Chromosomal DNA corresponding...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of neuro-oncology 1996-02, Vol.27 (2), p.111-115
Hauptverfasser: FINK, K. L, RUSHING, E. J, SCHOLD, S. C, NISEN, P. D
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 115
container_issue 2
container_start_page 111
container_title Journal of neuro-oncology
container_volume 27
creator FINK, K. L
RUSHING, E. J
SCHOLD, S. C
NISEN, P. D
description Ependymomas, which comprise 5% of central nervous system tumors, have not been extensively characterized genetically. The p53 tumor suppressor gene is frequently mutated in human cancer, and is important in the pathogenesis of other central nervous system (CNS) tumors. Chromosomal DNA corresponding to the p53 tumor suppressor gene was amplified by the polymerase chain reaction (PCR) from 31 archival ependymoma specimens. DNA was screened for the presence of p53 mutations by single strand conformational polymorphism (SSCP) analysis; samples with altered mobility were further tested for the presence of mutation by direct DNA sequence analysis. Of the 31 ependymomas tested, one contained a detectable DNA sequence change in the p53 gene. Sequencing revealed a silent mutation in exon 6, at codon 213, which represents a known p53 sequence polymorphism. These finding suggest that in contrast to many other human cancers, p53 mutation is not important in the pathogenesis or progression of ependymomas.
doi_str_mv 10.1007/bf00177473
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_78072638</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>78072638</sourcerecordid><originalsourceid>FETCH-LOGICAL-c340t-c4ac60a0b98f3a47dc22f0b5b8b4133236430c274aaa17972715da2b6d4d3c763</originalsourceid><addsrcrecordid>eNo90EFLxDAQBeAgyrquXrwLPYgHoTrJpJn2qIurCwteFLyVNE2k0qa1aQ_7761s9TSH9_EYHmOXHO44AN0XDoATScIjtuQJYUxIeMyWwBXFSSY_TtlZCF8AMBm-YItUZZlAsWSw9a6336P1Zh-1LuoSjD6tt1EzDnqoWh-iyke2s77cN22jwzk7cboO9mK-K_a-eXpbv8S71-ft-mEXG5QwxEZqo0BDkaUOtaTSCOGgSIq0kBxRoJIIRpDUWnPKSBBPSi0KVcoSDSlcsZtDb9e303thyJsqGFvX2tt2DDmlQEJhOsHbAzR9G0JvXd71VaP7fc4h_50nf9z8zTPhq7l1LBpb_tN5jym_nnMdjK5dr72pwj8TWaoQAX8ADWxqXw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>78072638</pqid></control><display><type>article</type><title>Infrequency of p53 gene mutations in ependymomas</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>FINK, K. L ; RUSHING, E. J ; SCHOLD, S. C ; NISEN, P. D</creator><creatorcontrib>FINK, K. L ; RUSHING, E. J ; SCHOLD, S. C ; NISEN, P. D</creatorcontrib><description>Ependymomas, which comprise 5% of central nervous system tumors, have not been extensively characterized genetically. The p53 tumor suppressor gene is frequently mutated in human cancer, and is important in the pathogenesis of other central nervous system (CNS) tumors. Chromosomal DNA corresponding to the p53 tumor suppressor gene was amplified by the polymerase chain reaction (PCR) from 31 archival ependymoma specimens. DNA was screened for the presence of p53 mutations by single strand conformational polymorphism (SSCP) analysis; samples with altered mobility were further tested for the presence of mutation by direct DNA sequence analysis. Of the 31 ependymomas tested, one contained a detectable DNA sequence change in the p53 gene. Sequencing revealed a silent mutation in exon 6, at codon 213, which represents a known p53 sequence polymorphism. These finding suggest that in contrast to many other human cancers, p53 mutation is not important in the pathogenesis or progression of ependymomas.</description><identifier>ISSN: 0167-594X</identifier><identifier>EISSN: 1573-7373</identifier><identifier>DOI: 10.1007/bf00177473</identifier><identifier>PMID: 8699232</identifier><identifier>CODEN: JNODD2</identifier><language>eng</language><publisher>Dordrecht: Springer</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Base Sequence ; Biological and medical sciences ; Brain Neoplasms - genetics ; Child ; Child, Preschool ; Ependymoma - genetics ; Female ; Genes, p53 ; Humans ; Infant ; Male ; Medical sciences ; Middle Aged ; Molecular Sequence Data ; Neurology ; Point Mutation ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; Tumors of the nervous system. Phacomatoses</subject><ispartof>Journal of neuro-oncology, 1996-02, Vol.27 (2), p.111-115</ispartof><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c340t-c4ac60a0b98f3a47dc22f0b5b8b4133236430c274aaa17972715da2b6d4d3c763</citedby><cites>FETCH-LOGICAL-c340t-c4ac60a0b98f3a47dc22f0b5b8b4133236430c274aaa17972715da2b6d4d3c763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=2986330$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8699232$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FINK, K. L</creatorcontrib><creatorcontrib>RUSHING, E. J</creatorcontrib><creatorcontrib>SCHOLD, S. C</creatorcontrib><creatorcontrib>NISEN, P. D</creatorcontrib><title>Infrequency of p53 gene mutations in ependymomas</title><title>Journal of neuro-oncology</title><addtitle>J Neurooncol</addtitle><description>Ependymomas, which comprise 5% of central nervous system tumors, have not been extensively characterized genetically. The p53 tumor suppressor gene is frequently mutated in human cancer, and is important in the pathogenesis of other central nervous system (CNS) tumors. Chromosomal DNA corresponding to the p53 tumor suppressor gene was amplified by the polymerase chain reaction (PCR) from 31 archival ependymoma specimens. DNA was screened for the presence of p53 mutations by single strand conformational polymorphism (SSCP) analysis; samples with altered mobility were further tested for the presence of mutation by direct DNA sequence analysis. Of the 31 ependymomas tested, one contained a detectable DNA sequence change in the p53 gene. Sequencing revealed a silent mutation in exon 6, at codon 213, which represents a known p53 sequence polymorphism. These finding suggest that in contrast to many other human cancers, p53 mutation is not important in the pathogenesis or progression of ependymomas.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Brain Neoplasms - genetics</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Ependymoma - genetics</subject><subject>Female</subject><subject>Genes, p53</subject><subject>Humans</subject><subject>Infant</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Molecular Sequence Data</subject><subject>Neurology</subject><subject>Point Mutation</subject><subject>Polymerase Chain Reaction</subject><subject>Polymorphism, Single-Stranded Conformational</subject><subject>Tumors of the nervous system. Phacomatoses</subject><issn>0167-594X</issn><issn>1573-7373</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo90EFLxDAQBeAgyrquXrwLPYgHoTrJpJn2qIurCwteFLyVNE2k0qa1aQ_7761s9TSH9_EYHmOXHO44AN0XDoATScIjtuQJYUxIeMyWwBXFSSY_TtlZCF8AMBm-YItUZZlAsWSw9a6336P1Zh-1LuoSjD6tt1EzDnqoWh-iyke2s77cN22jwzk7cboO9mK-K_a-eXpbv8S71-ft-mEXG5QwxEZqo0BDkaUOtaTSCOGgSIq0kBxRoJIIRpDUWnPKSBBPSi0KVcoSDSlcsZtDb9e303thyJsqGFvX2tt2DDmlQEJhOsHbAzR9G0JvXd71VaP7fc4h_50nf9z8zTPhq7l1LBpb_tN5jym_nnMdjK5dr72pwj8TWaoQAX8ADWxqXw</recordid><startdate>19960201</startdate><enddate>19960201</enddate><creator>FINK, K. L</creator><creator>RUSHING, E. J</creator><creator>SCHOLD, S. C</creator><creator>NISEN, P. D</creator><general>Springer</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19960201</creationdate><title>Infrequency of p53 gene mutations in ependymomas</title><author>FINK, K. L ; RUSHING, E. J ; SCHOLD, S. C ; NISEN, P. D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c340t-c4ac60a0b98f3a47dc22f0b5b8b4133236430c274aaa17972715da2b6d4d3c763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Brain Neoplasms - genetics</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Ependymoma - genetics</topic><topic>Female</topic><topic>Genes, p53</topic><topic>Humans</topic><topic>Infant</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Molecular Sequence Data</topic><topic>Neurology</topic><topic>Point Mutation</topic><topic>Polymerase Chain Reaction</topic><topic>Polymorphism, Single-Stranded Conformational</topic><topic>Tumors of the nervous system. Phacomatoses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FINK, K. L</creatorcontrib><creatorcontrib>RUSHING, E. J</creatorcontrib><creatorcontrib>SCHOLD, S. C</creatorcontrib><creatorcontrib>NISEN, P. D</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuro-oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FINK, K. L</au><au>RUSHING, E. J</au><au>SCHOLD, S. C</au><au>NISEN, P. D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Infrequency of p53 gene mutations in ependymomas</atitle><jtitle>Journal of neuro-oncology</jtitle><addtitle>J Neurooncol</addtitle><date>1996-02-01</date><risdate>1996</risdate><volume>27</volume><issue>2</issue><spage>111</spage><epage>115</epage><pages>111-115</pages><issn>0167-594X</issn><eissn>1573-7373</eissn><coden>JNODD2</coden><abstract>Ependymomas, which comprise 5% of central nervous system tumors, have not been extensively characterized genetically. The p53 tumor suppressor gene is frequently mutated in human cancer, and is important in the pathogenesis of other central nervous system (CNS) tumors. Chromosomal DNA corresponding to the p53 tumor suppressor gene was amplified by the polymerase chain reaction (PCR) from 31 archival ependymoma specimens. DNA was screened for the presence of p53 mutations by single strand conformational polymorphism (SSCP) analysis; samples with altered mobility were further tested for the presence of mutation by direct DNA sequence analysis. Of the 31 ependymomas tested, one contained a detectable DNA sequence change in the p53 gene. Sequencing revealed a silent mutation in exon 6, at codon 213, which represents a known p53 sequence polymorphism. These finding suggest that in contrast to many other human cancers, p53 mutation is not important in the pathogenesis or progression of ependymomas.</abstract><cop>Dordrecht</cop><pub>Springer</pub><pmid>8699232</pmid><doi>10.1007/bf00177473</doi><tpages>5</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0167-594X
ispartof Journal of neuro-oncology, 1996-02, Vol.27 (2), p.111-115
issn 0167-594X
1573-7373
language eng
recordid cdi_proquest_miscellaneous_78072638
source MEDLINE; SpringerNature Journals
subjects Adolescent
Adult
Aged
Aged, 80 and over
Base Sequence
Biological and medical sciences
Brain Neoplasms - genetics
Child
Child, Preschool
Ependymoma - genetics
Female
Genes, p53
Humans
Infant
Male
Medical sciences
Middle Aged
Molecular Sequence Data
Neurology
Point Mutation
Polymerase Chain Reaction
Polymorphism, Single-Stranded Conformational
Tumors of the nervous system. Phacomatoses
title Infrequency of p53 gene mutations in ependymomas
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-22T09%3A57%3A28IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Infrequency%20of%20p53%20gene%20mutations%20in%20ependymomas&rft.jtitle=Journal%20of%20neuro-oncology&rft.au=FINK,%20K.%20L&rft.date=1996-02-01&rft.volume=27&rft.issue=2&rft.spage=111&rft.epage=115&rft.pages=111-115&rft.issn=0167-594X&rft.eissn=1573-7373&rft.coden=JNODD2&rft_id=info:doi/10.1007/bf00177473&rft_dat=%3Cproquest_cross%3E78072638%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=78072638&rft_id=info:pmid/8699232&rfr_iscdi=true