Genome-wide linkage scan for atypical nevi in p16-Leiden melanoma families
In most Dutch melanoma families, a founder deletion in the melanoma susceptibility gene CDKN2A (which encodes p16) is present. This founder deletion (p16-Leiden) accounts for a significant proportion of the increased melanoma risk. However, it does not account for the Atypical Nevus (AN) phenotype t...
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| Veröffentlicht in: | European journal of human genetics : EJHG 2008-09, Vol.16 (9), p.1135-1141 |
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| creator | de Snoo, Femke A Hottenga, Jouke-Jan Gillanders, Elizabeth M Sandkuijl, Loudewijk A Jones, Mary Pat Bergman, Wilma van der Drift, Clasine van Leeuwen, Inge van Mourik, Lenny Huurne, Jeanet A C ter Frants, Rune R Willemze, Rein Breuning, Martijn H Trent, Jeffrey M Gruis, Nelleke A |
| description | In most Dutch melanoma families, a founder deletion in the melanoma susceptibility gene
CDKN2A
(which encodes p16) is present. This founder deletion (p16-Leiden) accounts for a significant proportion of the increased melanoma risk. However, it does not account for the Atypical Nevus (AN) phenotype that segregates in both p16-Leiden carriers and non-carriers. The AN-affected p16-Leiden family members are therefore a unique valuable resource for unraveling the genetic etiology of the AN phenotype, which is considered both a risk factor and a precursor lesion for melanoma. In this study, we performed a genome-wide scan for linkage in four p16-Leiden melanoma pedigrees, classifying family members with five or more AN as affected. The strongest evidence for an atypical nevus susceptibility gene was mapped to chromosome band 7q21.3 (two-point LOD score=2.751), a region containing candidate gene
CDK6
. |
| doi_str_mv | 10.1038/ejhg.2008.72 |
| format | Article |
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CDKN2A
(which encodes p16) is present. This founder deletion (p16-Leiden) accounts for a significant proportion of the increased melanoma risk. However, it does not account for the Atypical Nevus (AN) phenotype that segregates in both p16-Leiden carriers and non-carriers. The AN-affected p16-Leiden family members are therefore a unique valuable resource for unraveling the genetic etiology of the AN phenotype, which is considered both a risk factor and a precursor lesion for melanoma. In this study, we performed a genome-wide scan for linkage in four p16-Leiden melanoma pedigrees, classifying family members with five or more AN as affected. The strongest evidence for an atypical nevus susceptibility gene was mapped to chromosome band 7q21.3 (two-point LOD score=2.751), a region containing candidate gene
CDK6
.</description><identifier>ISSN: 1018-4813</identifier><identifier>EISSN: 1476-5438</identifier><identifier>DOI: 10.1038/ejhg.2008.72</identifier><identifier>PMID: 18398432</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Bioinformatics ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Cancer ; Chromosomes, Human, Pair 7 - genetics ; Classical genetics, quantitative genetics, hybrids ; Clonal deletion ; Cyclin-Dependent Kinase 6 - genetics ; Cytogenetics ; Dysplastic Nevus Syndrome - enzymology ; Dysplastic Nevus Syndrome - genetics ; Etiology ; Female ; Founder Effect ; Fundamental and applied biological sciences. Psychology ; Gene Deletion ; Gene Expression ; General aspects. Genetic counseling ; Genes, p16 ; Genetic Carrier Screening ; Genetic Linkage - genetics ; Genetic Predisposition to Disease ; Genetics ; Genetics of eukaryotes. Biological and molecular evolution ; Genomes ; Haplotypes ; Human ; Human Genetics ; Humans ; Investigations ; Male ; Medical genetics ; Medical sciences ; Melanoma ; Melanoma - enzymology ; Melanoma - genetics ; Molecular and cellular biology ; Mutation ; Nevus ; Pedigree ; Phenotypes ; Skin Neoplasms - enzymology ; Skin Neoplasms - genetics</subject><ispartof>European journal of human genetics : EJHG, 2008-09, Vol.16 (9), p.1135-1141</ispartof><rights>Macmillan Publishers Limited 2008</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Sep 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-936d71e0614b8e6138b2baa5df5da24758e1691c5276fc17de88d9093f8655153</citedby><cites>FETCH-LOGICAL-c478t-936d71e0614b8e6138b2baa5df5da24758e1691c5276fc17de88d9093f8655153</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ejhg.2008.72$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ejhg.2008.72$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20561725$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18398432$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de Snoo, Femke A</creatorcontrib><creatorcontrib>Hottenga, Jouke-Jan</creatorcontrib><creatorcontrib>Gillanders, Elizabeth M</creatorcontrib><creatorcontrib>Sandkuijl, Loudewijk A</creatorcontrib><creatorcontrib>Jones, Mary Pat</creatorcontrib><creatorcontrib>Bergman, Wilma</creatorcontrib><creatorcontrib>van der Drift, Clasine</creatorcontrib><creatorcontrib>van Leeuwen, Inge</creatorcontrib><creatorcontrib>van Mourik, Lenny</creatorcontrib><creatorcontrib>Huurne, Jeanet A C ter</creatorcontrib><creatorcontrib>Frants, Rune R</creatorcontrib><creatorcontrib>Willemze, Rein</creatorcontrib><creatorcontrib>Breuning, Martijn H</creatorcontrib><creatorcontrib>Trent, Jeffrey M</creatorcontrib><creatorcontrib>Gruis, Nelleke A</creatorcontrib><title>Genome-wide linkage scan for atypical nevi in p16-Leiden melanoma families</title><title>European journal of human genetics : EJHG</title><addtitle>Eur J Hum Genet</addtitle><addtitle>Eur J Hum Genet</addtitle><description>In most Dutch melanoma families, a founder deletion in the melanoma susceptibility gene
CDKN2A
(which encodes p16) is present. This founder deletion (p16-Leiden) accounts for a significant proportion of the increased melanoma risk. However, it does not account for the Atypical Nevus (AN) phenotype that segregates in both p16-Leiden carriers and non-carriers. The AN-affected p16-Leiden family members are therefore a unique valuable resource for unraveling the genetic etiology of the AN phenotype, which is considered both a risk factor and a precursor lesion for melanoma. In this study, we performed a genome-wide scan for linkage in four p16-Leiden melanoma pedigrees, classifying family members with five or more AN as affected. The strongest evidence for an atypical nevus susceptibility gene was mapped to chromosome band 7q21.3 (two-point LOD score=2.751), a region containing candidate gene
CDK6
.</description><subject>Bioinformatics</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer</subject><subject>Chromosomes, Human, Pair 7 - genetics</subject><subject>Classical genetics, quantitative genetics, hybrids</subject><subject>Clonal deletion</subject><subject>Cyclin-Dependent Kinase 6 - genetics</subject><subject>Cytogenetics</subject><subject>Dysplastic Nevus Syndrome - enzymology</subject><subject>Dysplastic Nevus Syndrome - genetics</subject><subject>Etiology</subject><subject>Female</subject><subject>Founder Effect</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Deletion</subject><subject>Gene Expression</subject><subject>General aspects. Genetic counseling</subject><subject>Genes, p16</subject><subject>Genetic Carrier Screening</subject><subject>Genetic Linkage - genetics</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetics</subject><subject>Genetics of eukaryotes. Biological and molecular evolution</subject><subject>Genomes</subject><subject>Haplotypes</subject><subject>Human</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Investigations</subject><subject>Male</subject><subject>Medical genetics</subject><subject>Medical sciences</subject><subject>Melanoma</subject><subject>Melanoma - enzymology</subject><subject>Melanoma - genetics</subject><subject>Molecular and cellular biology</subject><subject>Mutation</subject><subject>Nevus</subject><subject>Pedigree</subject><subject>Phenotypes</subject><subject>Skin Neoplasms - enzymology</subject><subject>Skin Neoplasms - genetics</subject><issn>1018-4813</issn><issn>1476-5438</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqF0c9rFDEUB_AgFlurN88SBD05a15-z1GKVstCL3oO2Zk3a9aZzJrsKP3vm7BLC4J4SiCffPNeHiGvgK2ACfsBdz-2K86YXRn-hFyANLpRUtinZc_ANtKCOCfPc94xVg4NPCPnYEVrpeAX5OYa4zxh8yf0SMcQf_ot0tz5SIc5UX-424fOjzTi70BDpHvQzRqLjXTC0Zerng5-CmPA_IKcDX7M-PK0XpLvnz99u_rSrG-vv159XDedNPbQtEL3BpBpkBuLGoTd8I33qh9U77k0yiLoFjrFjR46MD1a27esFYPVSoESl-TdMXef5l8L5oObQu5wLOXgvGSnW1nuAv8v5KyVUklW4Ju_4G5eUixNOA6mPstq2vsj6tKcc8LB7VOYfLpzwFydhKuTcHUSzlT--pS5bCbsH_Hp6wt4ewK-_Pc4JB-7kB8cZ0qD4bXd5uhyOYpbTI_F_eNhevTRH5aED4EVVVPIPYKXqK4</recordid><startdate>20080901</startdate><enddate>20080901</enddate><creator>de Snoo, Femke A</creator><creator>Hottenga, Jouke-Jan</creator><creator>Gillanders, Elizabeth M</creator><creator>Sandkuijl, Loudewijk A</creator><creator>Jones, Mary Pat</creator><creator>Bergman, Wilma</creator><creator>van der Drift, Clasine</creator><creator>van Leeuwen, Inge</creator><creator>van Mourik, Lenny</creator><creator>Huurne, Jeanet A C ter</creator><creator>Frants, Rune R</creator><creator>Willemze, Rein</creator><creator>Breuning, Martijn H</creator><creator>Trent, Jeffrey M</creator><creator>Gruis, Nelleke A</creator><general>Springer International Publishing</general><general>Nature Publishing</general><general>Nature Publishing Group</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20080901</creationdate><title>Genome-wide linkage scan for atypical nevi in p16-Leiden melanoma families</title><author>de Snoo, Femke A ; Hottenga, Jouke-Jan ; Gillanders, Elizabeth M ; Sandkuijl, Loudewijk A ; Jones, Mary Pat ; Bergman, Wilma ; van der Drift, Clasine ; van Leeuwen, Inge ; van Mourik, Lenny ; Huurne, Jeanet A C ter ; Frants, Rune R ; Willemze, Rein ; Breuning, Martijn H ; Trent, Jeffrey M ; Gruis, Nelleke A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-936d71e0614b8e6138b2baa5df5da24758e1691c5276fc17de88d9093f8655153</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Bioinformatics</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer</topic><topic>Chromosomes, Human, Pair 7 - genetics</topic><topic>Classical genetics, quantitative genetics, hybrids</topic><topic>Clonal deletion</topic><topic>Cyclin-Dependent Kinase 6 - genetics</topic><topic>Cytogenetics</topic><topic>Dysplastic Nevus Syndrome - enzymology</topic><topic>Dysplastic Nevus Syndrome - genetics</topic><topic>Etiology</topic><topic>Female</topic><topic>Founder Effect</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Deletion</topic><topic>Gene Expression</topic><topic>General aspects. Genetic counseling</topic><topic>Genes, p16</topic><topic>Genetic Carrier Screening</topic><topic>Genetic Linkage - genetics</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetics</topic><topic>Genetics of eukaryotes. Biological and molecular evolution</topic><topic>Genomes</topic><topic>Haplotypes</topic><topic>Human</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Investigations</topic><topic>Male</topic><topic>Medical genetics</topic><topic>Medical sciences</topic><topic>Melanoma</topic><topic>Melanoma - enzymology</topic><topic>Melanoma - genetics</topic><topic>Molecular and cellular biology</topic><topic>Mutation</topic><topic>Nevus</topic><topic>Pedigree</topic><topic>Phenotypes</topic><topic>Skin Neoplasms - enzymology</topic><topic>Skin Neoplasms - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de Snoo, Femke A</creatorcontrib><creatorcontrib>Hottenga, Jouke-Jan</creatorcontrib><creatorcontrib>Gillanders, Elizabeth M</creatorcontrib><creatorcontrib>Sandkuijl, Loudewijk A</creatorcontrib><creatorcontrib>Jones, Mary Pat</creatorcontrib><creatorcontrib>Bergman, Wilma</creatorcontrib><creatorcontrib>van der Drift, Clasine</creatorcontrib><creatorcontrib>van Leeuwen, Inge</creatorcontrib><creatorcontrib>van Mourik, Lenny</creatorcontrib><creatorcontrib>Huurne, Jeanet A C ter</creatorcontrib><creatorcontrib>Frants, Rune R</creatorcontrib><creatorcontrib>Willemze, Rein</creatorcontrib><creatorcontrib>Breuning, Martijn H</creatorcontrib><creatorcontrib>Trent, Jeffrey M</creatorcontrib><creatorcontrib>Gruis, Nelleke A</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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of human genetics : EJHG</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de Snoo, Femke A</au><au>Hottenga, Jouke-Jan</au><au>Gillanders, Elizabeth M</au><au>Sandkuijl, Loudewijk A</au><au>Jones, Mary Pat</au><au>Bergman, Wilma</au><au>van der Drift, Clasine</au><au>van Leeuwen, Inge</au><au>van Mourik, Lenny</au><au>Huurne, Jeanet A C ter</au><au>Frants, Rune R</au><au>Willemze, Rein</au><au>Breuning, Martijn H</au><au>Trent, Jeffrey M</au><au>Gruis, Nelleke A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genome-wide linkage scan for atypical nevi in p16-Leiden melanoma families</atitle><jtitle>European journal of human genetics : EJHG</jtitle><stitle>Eur J Hum Genet</stitle><addtitle>Eur J Hum Genet</addtitle><date>2008-09-01</date><risdate>2008</risdate><volume>16</volume><issue>9</issue><spage>1135</spage><epage>1141</epage><pages>1135-1141</pages><issn>1018-4813</issn><eissn>1476-5438</eissn><abstract>In most Dutch melanoma families, a founder deletion in the melanoma susceptibility gene
CDKN2A
(which encodes p16) is present. This founder deletion (p16-Leiden) accounts for a significant proportion of the increased melanoma risk. However, it does not account for the Atypical Nevus (AN) phenotype that segregates in both p16-Leiden carriers and non-carriers. The AN-affected p16-Leiden family members are therefore a unique valuable resource for unraveling the genetic etiology of the AN phenotype, which is considered both a risk factor and a precursor lesion for melanoma. In this study, we performed a genome-wide scan for linkage in four p16-Leiden melanoma pedigrees, classifying family members with five or more AN as affected. The strongest evidence for an atypical nevus susceptibility gene was mapped to chromosome band 7q21.3 (two-point LOD score=2.751), a region containing candidate gene
CDK6
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| ispartof | European journal of human genetics : EJHG, 2008-09, Vol.16 (9), p.1135-1141 |
| issn | 1018-4813 1476-5438 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SpringerLink Journals - AutoHoldings |
| subjects | Bioinformatics Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Chromosomes, Human, Pair 7 - genetics Classical genetics, quantitative genetics, hybrids Clonal deletion Cyclin-Dependent Kinase 6 - genetics Cytogenetics Dysplastic Nevus Syndrome - enzymology Dysplastic Nevus Syndrome - genetics Etiology Female Founder Effect Fundamental and applied biological sciences. Psychology Gene Deletion Gene Expression General aspects. Genetic counseling Genes, p16 Genetic Carrier Screening Genetic Linkage - genetics Genetic Predisposition to Disease Genetics Genetics of eukaryotes. Biological and molecular evolution Genomes Haplotypes Human Human Genetics Humans Investigations Male Medical genetics Medical sciences Melanoma Melanoma - enzymology Melanoma - genetics Molecular and cellular biology Mutation Nevus Pedigree Phenotypes Skin Neoplasms - enzymology Skin Neoplasms - genetics |
| title | Genome-wide linkage scan for atypical nevi in p16-Leiden melanoma families |
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