Relationship between FRA11F and 11q13 gene amplification in oral cancer

Common fragile sites (CFS) are nonstaining gaps or breaks in chromosomes that are expressed under conditions inducing replicative stress. CFS have been suggested to play a role in epithelial cancers by their association with loss of heterozygosity, loss of gene expression, and/or gene amplification...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Genes chromosomes & cancer 2007-02, Vol.46 (2), p.143-154
Hauptverfasser: Reshmi, Shalini C., Huang, Xin, Schoppy, David W., Black, Robert C., Saunders, William S., Smith, David I., Gollin, Susanne M.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 154
container_issue 2
container_start_page 143
container_title Genes chromosomes & cancer
container_volume 46
creator Reshmi, Shalini C.
Huang, Xin
Schoppy, David W.
Black, Robert C.
Saunders, William S.
Smith, David I.
Gollin, Susanne M.
description Common fragile sites (CFS) are nonstaining gaps or breaks in chromosomes that are expressed under conditions inducing replicative stress. CFS have been suggested to play a role in epithelial cancers by their association with loss of heterozygosity, loss of gene expression, and/or gene amplification in the form of homogeneously staining regions (hsrs). In oral squamous‐cell carcinomas (OSCC), amplification of chromosomal band 11q13 occurs in the form of an hsr. We suggested previously that CFS flanking 11q13 may be susceptible to breakage induced by tobacco or other carcinogens and/or human papillomavirus, promoting formation of the 11q13 amplicon. Examination of OSCC cell lines with 11q13 amplification using fluorescence in situ hybridization showed loss of FRA11F sequences, whereas cell lines without 11q13 amplification displayed an intact FRA11F site. Cell lines with more complex 11q rearrangements expressed FRA11F in the form of an inverted duplication, characteristic of breakage‐fusion‐bridge cycles. Our findings suggest that gene amplification involving chromosomal band 11q13 in OSCC may be initiated by breakage at FRA11F. © 2006 Wiley‐Liss, Inc.
doi_str_mv 10.1002/gcc.20394
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_20444125</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20444125</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3924-ad4ea92aea4ec4ae0e3061ac8f773eab1af447be19888945c77eee836eccff9e3</originalsourceid><addsrcrecordid>eNp1kEtPAjEURhujEUUX_gHTlYmLgXbambZLQgRNiCb4YNlcyh2sDjMwhSD_3uGhrlzduzjfWRxCrjhrccbi9tS5VsyEkUfkjDOjozhO5fH2l0n9J6pBzkP4YIylwiSnpMEVM0Yrfkb6Q8xh6csivPs5HeNyjVjQ3rDDeY9CMaGcL7igUyyQwmye-8y7HU99QcsKcuqgcFhdkJMM8oCXh9skr727l-59NHjqP3Q7g8gJE8sIJhLBxIAg0UlAhoKlHJzOlBIIYw6ZlGqM3GitjUycUoioRYrOZZlB0SQ3e--8KhcrDEs788FhnkOB5SrYmEkpeZzU4O0edFUZQoWZnVd-BtXGcma31Wxdze6q1ez1Qboaz3DyRx4y1UB7D6x9jpv_Tbbf7f4oo_3ChyV-_S6g-rSpEiqxo8e-fR7qt146ElaLb-xPhKY</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>20444125</pqid></control><display><type>article</type><title>Relationship between FRA11F and 11q13 gene amplification in oral cancer</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Reshmi, Shalini C. ; Huang, Xin ; Schoppy, David W. ; Black, Robert C. ; Saunders, William S. ; Smith, David I. ; Gollin, Susanne M.</creator><creatorcontrib>Reshmi, Shalini C. ; Huang, Xin ; Schoppy, David W. ; Black, Robert C. ; Saunders, William S. ; Smith, David I. ; Gollin, Susanne M.</creatorcontrib><description>Common fragile sites (CFS) are nonstaining gaps or breaks in chromosomes that are expressed under conditions inducing replicative stress. CFS have been suggested to play a role in epithelial cancers by their association with loss of heterozygosity, loss of gene expression, and/or gene amplification in the form of homogeneously staining regions (hsrs). In oral squamous‐cell carcinomas (OSCC), amplification of chromosomal band 11q13 occurs in the form of an hsr. We suggested previously that CFS flanking 11q13 may be susceptible to breakage induced by tobacco or other carcinogens and/or human papillomavirus, promoting formation of the 11q13 amplicon. Examination of OSCC cell lines with 11q13 amplification using fluorescence in situ hybridization showed loss of FRA11F sequences, whereas cell lines without 11q13 amplification displayed an intact FRA11F site. Cell lines with more complex 11q rearrangements expressed FRA11F in the form of an inverted duplication, characteristic of breakage‐fusion‐bridge cycles. Our findings suggest that gene amplification involving chromosomal band 11q13 in OSCC may be initiated by breakage at FRA11F. © 2006 Wiley‐Liss, Inc.</description><identifier>ISSN: 1045-2257</identifier><identifier>EISSN: 1098-2264</identifier><identifier>DOI: 10.1002/gcc.20394</identifier><identifier>PMID: 17099871</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Carcinoma, Squamous Cell - genetics ; Cell Line, Tumor ; Chromosome Banding ; Chromosome Breakage ; Chromosomes, Human, Pair 11 - genetics ; Gene Amplification ; Genetic Markers ; Human papillomavirus ; Humans ; Mouth Neoplasms - genetics</subject><ispartof>Genes chromosomes &amp; cancer, 2007-02, Vol.46 (2), p.143-154</ispartof><rights>Copyright © 2006 Wiley‐Liss, Inc.</rights><rights>Copyright 2006 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3924-ad4ea92aea4ec4ae0e3061ac8f773eab1af447be19888945c77eee836eccff9e3</citedby><cites>FETCH-LOGICAL-c3924-ad4ea92aea4ec4ae0e3061ac8f773eab1af447be19888945c77eee836eccff9e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fgcc.20394$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fgcc.20394$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17099871$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reshmi, Shalini C.</creatorcontrib><creatorcontrib>Huang, Xin</creatorcontrib><creatorcontrib>Schoppy, David W.</creatorcontrib><creatorcontrib>Black, Robert C.</creatorcontrib><creatorcontrib>Saunders, William S.</creatorcontrib><creatorcontrib>Smith, David I.</creatorcontrib><creatorcontrib>Gollin, Susanne M.</creatorcontrib><title>Relationship between FRA11F and 11q13 gene amplification in oral cancer</title><title>Genes chromosomes &amp; cancer</title><addtitle>Genes Chromosom. Cancer</addtitle><description>Common fragile sites (CFS) are nonstaining gaps or breaks in chromosomes that are expressed under conditions inducing replicative stress. CFS have been suggested to play a role in epithelial cancers by their association with loss of heterozygosity, loss of gene expression, and/or gene amplification in the form of homogeneously staining regions (hsrs). In oral squamous‐cell carcinomas (OSCC), amplification of chromosomal band 11q13 occurs in the form of an hsr. We suggested previously that CFS flanking 11q13 may be susceptible to breakage induced by tobacco or other carcinogens and/or human papillomavirus, promoting formation of the 11q13 amplicon. Examination of OSCC cell lines with 11q13 amplification using fluorescence in situ hybridization showed loss of FRA11F sequences, whereas cell lines without 11q13 amplification displayed an intact FRA11F site. Cell lines with more complex 11q rearrangements expressed FRA11F in the form of an inverted duplication, characteristic of breakage‐fusion‐bridge cycles. Our findings suggest that gene amplification involving chromosomal band 11q13 in OSCC may be initiated by breakage at FRA11F. © 2006 Wiley‐Liss, Inc.</description><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Cell Line, Tumor</subject><subject>Chromosome Banding</subject><subject>Chromosome Breakage</subject><subject>Chromosomes, Human, Pair 11 - genetics</subject><subject>Gene Amplification</subject><subject>Genetic Markers</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>Mouth Neoplasms - genetics</subject><issn>1045-2257</issn><issn>1098-2264</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEtPAjEURhujEUUX_gHTlYmLgXbambZLQgRNiCb4YNlcyh2sDjMwhSD_3uGhrlzduzjfWRxCrjhrccbi9tS5VsyEkUfkjDOjozhO5fH2l0n9J6pBzkP4YIylwiSnpMEVM0Yrfkb6Q8xh6csivPs5HeNyjVjQ3rDDeY9CMaGcL7igUyyQwmye-8y7HU99QcsKcuqgcFhdkJMM8oCXh9skr727l-59NHjqP3Q7g8gJE8sIJhLBxIAg0UlAhoKlHJzOlBIIYw6ZlGqM3GitjUycUoioRYrOZZlB0SQ3e--8KhcrDEs788FhnkOB5SrYmEkpeZzU4O0edFUZQoWZnVd-BtXGcma31Wxdze6q1ez1Qboaz3DyRx4y1UB7D6x9jpv_Tbbf7f4oo_3ChyV-_S6g-rSpEiqxo8e-fR7qt146ElaLb-xPhKY</recordid><startdate>200702</startdate><enddate>200702</enddate><creator>Reshmi, Shalini C.</creator><creator>Huang, Xin</creator><creator>Schoppy, David W.</creator><creator>Black, Robert C.</creator><creator>Saunders, William S.</creator><creator>Smith, David I.</creator><creator>Gollin, Susanne M.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</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>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>200702</creationdate><title>Relationship between FRA11F and 11q13 gene amplification in oral cancer</title><author>Reshmi, Shalini C. ; Huang, Xin ; Schoppy, David W. ; Black, Robert C. ; Saunders, William S. ; Smith, David I. ; Gollin, Susanne M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3924-ad4ea92aea4ec4ae0e3061ac8f773eab1af447be19888945c77eee836eccff9e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Cell Line, Tumor</topic><topic>Chromosome Banding</topic><topic>Chromosome Breakage</topic><topic>Chromosomes, Human, Pair 11 - genetics</topic><topic>Gene Amplification</topic><topic>Genetic Markers</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>Mouth Neoplasms - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Reshmi, Shalini C.</creatorcontrib><creatorcontrib>Huang, Xin</creatorcontrib><creatorcontrib>Schoppy, David W.</creatorcontrib><creatorcontrib>Black, Robert C.</creatorcontrib><creatorcontrib>Saunders, William S.</creatorcontrib><creatorcontrib>Smith, David I.</creatorcontrib><creatorcontrib>Gollin, Susanne M.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Genes chromosomes &amp; cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Reshmi, Shalini C.</au><au>Huang, Xin</au><au>Schoppy, David W.</au><au>Black, Robert C.</au><au>Saunders, William S.</au><au>Smith, David I.</au><au>Gollin, Susanne M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Relationship between FRA11F and 11q13 gene amplification in oral cancer</atitle><jtitle>Genes chromosomes &amp; cancer</jtitle><addtitle>Genes Chromosom. Cancer</addtitle><date>2007-02</date><risdate>2007</risdate><volume>46</volume><issue>2</issue><spage>143</spage><epage>154</epage><pages>143-154</pages><issn>1045-2257</issn><eissn>1098-2264</eissn><abstract>Common fragile sites (CFS) are nonstaining gaps or breaks in chromosomes that are expressed under conditions inducing replicative stress. CFS have been suggested to play a role in epithelial cancers by their association with loss of heterozygosity, loss of gene expression, and/or gene amplification in the form of homogeneously staining regions (hsrs). In oral squamous‐cell carcinomas (OSCC), amplification of chromosomal band 11q13 occurs in the form of an hsr. We suggested previously that CFS flanking 11q13 may be susceptible to breakage induced by tobacco or other carcinogens and/or human papillomavirus, promoting formation of the 11q13 amplicon. Examination of OSCC cell lines with 11q13 amplification using fluorescence in situ hybridization showed loss of FRA11F sequences, whereas cell lines without 11q13 amplification displayed an intact FRA11F site. Cell lines with more complex 11q rearrangements expressed FRA11F in the form of an inverted duplication, characteristic of breakage‐fusion‐bridge cycles. Our findings suggest that gene amplification involving chromosomal band 11q13 in OSCC may be initiated by breakage at FRA11F. © 2006 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>17099871</pmid><doi>10.1002/gcc.20394</doi><tpages>12</tpages></addata></record>
fulltext fulltext
identifier ISSN: 1045-2257
ispartof Genes chromosomes & cancer, 2007-02, Vol.46 (2), p.143-154
issn 1045-2257
1098-2264
language eng
recordid cdi_proquest_miscellaneous_20444125
source MEDLINE; Access via Wiley Online Library
subjects Carcinoma, Squamous Cell - genetics
Cell Line, Tumor
Chromosome Banding
Chromosome Breakage
Chromosomes, Human, Pair 11 - genetics
Gene Amplification
Genetic Markers
Human papillomavirus
Humans
Mouth Neoplasms - genetics
title Relationship between FRA11F and 11q13 gene amplification in oral cancer
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T13%3A16%3A36IST&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=Relationship%20between%20FRA11F%20and%2011q13%20gene%20amplification%20in%20oral%20cancer&rft.jtitle=Genes%20chromosomes%20&%20cancer&rft.au=Reshmi,%20Shalini%20C.&rft.date=2007-02&rft.volume=46&rft.issue=2&rft.spage=143&rft.epage=154&rft.pages=143-154&rft.issn=1045-2257&rft.eissn=1098-2264&rft_id=info:doi/10.1002/gcc.20394&rft_dat=%3Cproquest_cross%3E20444125%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=20444125&rft_id=info:pmid/17099871&rfr_iscdi=true