c‐MYC Asn11Ser is associated with increased risk for familial breast cancer
c‐MYC is a multifaceted protein that regulates cell proliferation, differentiation and apoptosis. Its crucial role in diverse cancers has been demonstrated in several studies. Here, we analysed the influence of the rare c‐MYC Asn11Ser polymorphism on familial breast cancer risk by performing a case‐...
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| Veröffentlicht in: | International journal of cancer 2005-11, Vol.117 (4), p.638-642 |
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| creator | Wirtenberger, Michael Hemminki, Kari Försti, Asta Klaes, Rüdiger Schmutzler, Rita K. Grzybowska, Ewa Bermejo, Justo L. Wappenschmidt, Barbara Bugert, Peter Butkiewicz, Dorota Pamula, Jolanta Pekala, Wioletta Zientek, Helena Bartram, Claus R. Burwinkel, Barbara |
| description | c‐MYC is a multifaceted protein that regulates cell proliferation, differentiation and apoptosis. Its crucial role in diverse cancers has been demonstrated in several studies. Here, we analysed the influence of the rare c‐MYC Asn11Ser polymorphism on familial breast cancer risk by performing a case‐control study with a Polish (cases n = 349; controls n = 441) and a German (cases n = 356; controls n = 655) study population. All cases have been tested negative for mutations in the BRCA1 and BRCA2 genes. A joint analysis of the Polish and the German study population revealed a 54% increased risk for breast cancer associated with the heterozygous Asn11Ser variant (OR = 1.54, 95% CI 1.05–2.26, p = 0.028). The breast cancer risk associated with this genotype increases above the age of 50 years (OR = 2.24, 95% CI 1.20–4.21, p = 0.012). The wild‐type amino acid Asn of this polymorphism is located in the N‐terminal MYC transactivation domain and is highly conserved not only among most diverse species but also in the N‐MYC homologue. Due to the pivotal role of c‐MYC in diverse tumours, this variant might affect the genetic susceptibility of other cancers as well. © 2005 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/ijc.21225 |
| format | Article |
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Its crucial role in diverse cancers has been demonstrated in several studies. Here, we analysed the influence of the rare c‐MYC Asn11Ser polymorphism on familial breast cancer risk by performing a case‐control study with a Polish (cases n = 349; controls n = 441) and a German (cases n = 356; controls n = 655) study population. All cases have been tested negative for mutations in the BRCA1 and BRCA2 genes. A joint analysis of the Polish and the German study population revealed a 54% increased risk for breast cancer associated with the heterozygous Asn11Ser variant (OR = 1.54, 95% CI 1.05–2.26, p = 0.028). The breast cancer risk associated with this genotype increases above the age of 50 years (OR = 2.24, 95% CI 1.20–4.21, p = 0.012). The wild‐type amino acid Asn of this polymorphism is located in the N‐terminal MYC transactivation domain and is highly conserved not only among most diverse species but also in the N‐MYC homologue. Due to the pivotal role of c‐MYC in diverse tumours, this variant might affect the genetic susceptibility of other cancers as well. © 2005 Wiley‐Liss, Inc.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.21225</identifier><identifier>PMID: 15929079</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Amino Acid Sequence ; apoptosis ; Asparagine - genetics ; Biological and medical sciences ; breast cancer ; Breast Neoplasms - genetics ; case‐control study ; c‐MYC ; Female ; Genetic Predisposition to Disease ; Gynecology. Andrology. Obstetrics ; Humans ; Mammary gland diseases ; Medical sciences ; Molecular Sequence Data ; polymorphism ; Polymorphism, Single Nucleotide ; Proto-Oncogene Proteins c-myc - chemistry ; Proto-Oncogene Proteins c-myc - genetics ; Sequence Homology, Amino Acid ; Serine - genetics ; Tumors</subject><ispartof>International journal of cancer, 2005-11, Vol.117 (4), p.638-642</ispartof><rights>Copyright © 2005 Wiley‐Liss, Inc.</rights><rights>2005 INIST-CNRS</rights><rights>Copyright 2005 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3845-3e173c9d087527e598b1dc6b0586240dda76d34d35e9fdff45002720d7dbe5593</citedby><cites>FETCH-LOGICAL-c3845-3e173c9d087527e598b1dc6b0586240dda76d34d35e9fdff45002720d7dbe5593</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%2Fijc.21225$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fijc.21225$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17205791$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15929079$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wirtenberger, Michael</creatorcontrib><creatorcontrib>Hemminki, Kari</creatorcontrib><creatorcontrib>Försti, Asta</creatorcontrib><creatorcontrib>Klaes, Rüdiger</creatorcontrib><creatorcontrib>Schmutzler, Rita K.</creatorcontrib><creatorcontrib>Grzybowska, Ewa</creatorcontrib><creatorcontrib>Bermejo, Justo L.</creatorcontrib><creatorcontrib>Wappenschmidt, Barbara</creatorcontrib><creatorcontrib>Bugert, Peter</creatorcontrib><creatorcontrib>Butkiewicz, Dorota</creatorcontrib><creatorcontrib>Pamula, Jolanta</creatorcontrib><creatorcontrib>Pekala, Wioletta</creatorcontrib><creatorcontrib>Zientek, Helena</creatorcontrib><creatorcontrib>Bartram, Claus R.</creatorcontrib><creatorcontrib>Burwinkel, Barbara</creatorcontrib><title>c‐MYC Asn11Ser is associated with increased risk for familial breast cancer</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>c‐MYC is a multifaceted protein that regulates cell proliferation, differentiation and apoptosis. Its crucial role in diverse cancers has been demonstrated in several studies. Here, we analysed the influence of the rare c‐MYC Asn11Ser polymorphism on familial breast cancer risk by performing a case‐control study with a Polish (cases n = 349; controls n = 441) and a German (cases n = 356; controls n = 655) study population. All cases have been tested negative for mutations in the BRCA1 and BRCA2 genes. A joint analysis of the Polish and the German study population revealed a 54% increased risk for breast cancer associated with the heterozygous Asn11Ser variant (OR = 1.54, 95% CI 1.05–2.26, p = 0.028). The breast cancer risk associated with this genotype increases above the age of 50 years (OR = 2.24, 95% CI 1.20–4.21, p = 0.012). The wild‐type amino acid Asn of this polymorphism is located in the N‐terminal MYC transactivation domain and is highly conserved not only among most diverse species but also in the N‐MYC homologue. Due to the pivotal role of c‐MYC in diverse tumours, this variant might affect the genetic susceptibility of other cancers as well. © 2005 Wiley‐Liss, Inc.</description><subject>Amino Acid Sequence</subject><subject>apoptosis</subject><subject>Asparagine - genetics</subject><subject>Biological and medical sciences</subject><subject>breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>case‐control study</subject><subject>c‐MYC</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Molecular Sequence Data</subject><subject>polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Proto-Oncogene Proteins c-myc - chemistry</subject><subject>Proto-Oncogene Proteins c-myc - genetics</subject><subject>Sequence Homology, Amino Acid</subject><subject>Serine - genetics</subject><subject>Tumors</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0M1OAjEQB_DGaATRgy9getHEw8K02263R0L8wEA8qAdPm27bjcWFxRZCuPkIPqNPYhESTsbTZDK_zGT-CJ0T6BIA2nMT3aWEUn6A2gSkSIASfojacQaJIGnWQichTAAI4cCOUYtwSSUI2UZj_f35NX4d4H6YEfJkPXYBqxAa7dTCGrxyizfsZtpbFWLrXXjHVeNxpaaudqrG5WaywFrNtPWn6KhSdbBnu9pBL7c3z4P7ZPR4Nxz0R4lOc8aT1BKRamkgF5wKy2VeEqOzEnieUQbGKJGZlJmUW1mZqmI8fiIoGGFKy7lMO-hqu3fum4-lDYti6oK2da1mtlmGIsszYIyJfyEFQQRnWYTXW6h9E4K3VTH3bqr8uiBQbEIuYsjFb8jRXuyWLsupNXu5SzWCyx1QQau68jEcF_YuvsKFJNH1tm7larv--2IxfBhsT_8A7jCRpQ</recordid><startdate>20051120</startdate><enddate>20051120</enddate><creator>Wirtenberger, Michael</creator><creator>Hemminki, Kari</creator><creator>Försti, Asta</creator><creator>Klaes, Rüdiger</creator><creator>Schmutzler, Rita K.</creator><creator>Grzybowska, Ewa</creator><creator>Bermejo, Justo L.</creator><creator>Wappenschmidt, Barbara</creator><creator>Bugert, Peter</creator><creator>Butkiewicz, Dorota</creator><creator>Pamula, Jolanta</creator><creator>Pekala, Wioletta</creator><creator>Zientek, Helena</creator><creator>Bartram, Claus R.</creator><creator>Burwinkel, Barbara</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</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>7TO</scope><scope>7U1</scope><scope>7U2</scope><scope>C1K</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20051120</creationdate><title>c‐MYC Asn11Ser is associated with increased risk for familial breast cancer</title><author>Wirtenberger, Michael ; Hemminki, Kari ; Försti, Asta ; Klaes, Rüdiger ; Schmutzler, Rita K. ; Grzybowska, Ewa ; Bermejo, Justo L. ; Wappenschmidt, Barbara ; Bugert, Peter ; Butkiewicz, Dorota ; Pamula, Jolanta ; Pekala, Wioletta ; Zientek, Helena ; Bartram, Claus R. ; Burwinkel, Barbara</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3845-3e173c9d087527e598b1dc6b0586240dda76d34d35e9fdff45002720d7dbe5593</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Amino Acid Sequence</topic><topic>apoptosis</topic><topic>Asparagine - genetics</topic><topic>Biological and medical sciences</topic><topic>breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>case‐control study</topic><topic>c‐MYC</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Molecular Sequence Data</topic><topic>polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Proto-Oncogene Proteins c-myc - chemistry</topic><topic>Proto-Oncogene Proteins c-myc - genetics</topic><topic>Sequence Homology, Amino Acid</topic><topic>Serine - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wirtenberger, Michael</creatorcontrib><creatorcontrib>Hemminki, Kari</creatorcontrib><creatorcontrib>Försti, Asta</creatorcontrib><creatorcontrib>Klaes, Rüdiger</creatorcontrib><creatorcontrib>Schmutzler, Rita K.</creatorcontrib><creatorcontrib>Grzybowska, Ewa</creatorcontrib><creatorcontrib>Bermejo, Justo L.</creatorcontrib><creatorcontrib>Wappenschmidt, Barbara</creatorcontrib><creatorcontrib>Bugert, Peter</creatorcontrib><creatorcontrib>Butkiewicz, Dorota</creatorcontrib><creatorcontrib>Pamula, Jolanta</creatorcontrib><creatorcontrib>Pekala, Wioletta</creatorcontrib><creatorcontrib>Zientek, Helena</creatorcontrib><creatorcontrib>Bartram, Claus R.</creatorcontrib><creatorcontrib>Burwinkel, Barbara</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>Oncogenes and Growth Factors Abstracts</collection><collection>Risk Abstracts</collection><collection>Safety Science and Risk</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wirtenberger, Michael</au><au>Hemminki, Kari</au><au>Försti, Asta</au><au>Klaes, Rüdiger</au><au>Schmutzler, Rita K.</au><au>Grzybowska, Ewa</au><au>Bermejo, Justo L.</au><au>Wappenschmidt, Barbara</au><au>Bugert, Peter</au><au>Butkiewicz, Dorota</au><au>Pamula, Jolanta</au><au>Pekala, Wioletta</au><au>Zientek, Helena</au><au>Bartram, Claus R.</au><au>Burwinkel, Barbara</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>c‐MYC Asn11Ser is associated with increased risk for familial breast cancer</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>2005-11-20</date><risdate>2005</risdate><volume>117</volume><issue>4</issue><spage>638</spage><epage>642</epage><pages>638-642</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><coden>IJCNAW</coden><abstract>c‐MYC is a multifaceted protein that regulates cell proliferation, differentiation and apoptosis. Its crucial role in diverse cancers has been demonstrated in several studies. Here, we analysed the influence of the rare c‐MYC Asn11Ser polymorphism on familial breast cancer risk by performing a case‐control study with a Polish (cases n = 349; controls n = 441) and a German (cases n = 356; controls n = 655) study population. All cases have been tested negative for mutations in the BRCA1 and BRCA2 genes. A joint analysis of the Polish and the German study population revealed a 54% increased risk for breast cancer associated with the heterozygous Asn11Ser variant (OR = 1.54, 95% CI 1.05–2.26, p = 0.028). The breast cancer risk associated with this genotype increases above the age of 50 years (OR = 2.24, 95% CI 1.20–4.21, p = 0.012). The wild‐type amino acid Asn of this polymorphism is located in the N‐terminal MYC transactivation domain and is highly conserved not only among most diverse species but also in the N‐MYC homologue. Due to the pivotal role of c‐MYC in diverse tumours, this variant might affect the genetic susceptibility of other cancers as well. © 2005 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>15929079</pmid><doi>10.1002/ijc.21225</doi><tpages>5</tpages></addata></record> |
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| subjects | Amino Acid Sequence apoptosis Asparagine - genetics Biological and medical sciences breast cancer Breast Neoplasms - genetics case‐control study c‐MYC Female Genetic Predisposition to Disease Gynecology. Andrology. Obstetrics Humans Mammary gland diseases Medical sciences Molecular Sequence Data polymorphism Polymorphism, Single Nucleotide Proto-Oncogene Proteins c-myc - chemistry Proto-Oncogene Proteins c-myc - genetics Sequence Homology, Amino Acid Serine - genetics Tumors |
| title | c‐MYC Asn11Ser is associated with increased risk for familial breast cancer |
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