Genetic Variants in CCNB1 Associated With Differential Gene Transcription and Risk of Coronary In-Stent Restenosis
BACKGROUND—The development of diagnostic tools to assess restenosis risk after stent deployment may enable the intervention to be tailored to the individual patient, for example, by targeting the use of drug-eluting stent to high-risk patients, with the goal of improving safety and reducing costs. T...
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| Veröffentlicht in: | Circulation. Cardiovascular genetics 2014-02, Vol.7 (1), p.59-70 |
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| creator | Silvestre-Roig, Carlos Fernández, Patricia Mansego, María L van Tiel, Claudia M Viana, Rosa Anselmi, Chiara Viviani Condorelli, Gianluigi de Winter, Robbert J Martín-Fuentes, Paula Solanas-Barca, María Civeira, Fernando Focaccio, Amelia de Vries, Carlie J.M Chaves, Felipe Javier Andrés, Vicente |
| description | BACKGROUND—The development of diagnostic tools to assess restenosis risk after stent deployment may enable the intervention to be tailored to the individual patient, for example, by targeting the use of drug-eluting stent to high-risk patients, with the goal of improving safety and reducing costs. The CCNB1 gene (encoding cyclin B1) positively regulates cell proliferation, a key component of in-stent restenosis. Therefore, we hypothesized that single-nucleotide polymorphisms in CCNB1 may serve as useful tools in risk stratification for in-stent restenosis.
METHODS AND RESULTS—We identified 3 single-nucleotide polymorphisms in CCNB1 associated with increased restenosis risk in a cohort of 284 patients undergoing coronary angioplasty and stent placement (rs350099TT versus CC+TC; odds ratio [OR], 1.82; 95% confidence interval [CI], 1.09–3.03; P=0.023; rs350104CC versus CT+TT; OR, 1.82; 95% CI, 1.02–3.26; P=0.040; and rs164390GG versus GT+TT; OR, 2.27; 95% CI, 1.33–3.85; P=0.002). These findings were replicated in another cohort study of 715 patients (rs350099TT versus CC+TC; OR, 1.88; 95% CI, 0.92–3.81; P=0.080; rs350104CC versus CT+TT; OR, 2.23; 95% CI, 1.18–4.25; P=0.016; and rs164390GG versus GT+TT; OR, 1.87; 95% CI, 1.03–3.47; P=0.040). Moreover, the haplotype containing all 3 risk alleles is associated with higher CCNB1 mRNA expression in circulating lymphocytes and increased in-stent restenosis risk (OR, 1.43; 95% CI, 1.00–1.823; P=0.039). The risk variants of rs350099, rs350104, and rs164390 are associated with increased reporter gene expression through binding of transcription factors nuclear factor-Y, activator protein 1, and specificity protein 1, respectively.
CONCLUSIONS—Allele-dependent transcriptional regulation of CCNB1 associated with rs350099, rs350104, and rs164390 affects the risk of in-stent restenosis. These findings reveal these common genetic variations as attractive diagnostic tools in risk stratification for restenosis. |
| doi_str_mv | 10.1161/CIRCGENETICS.113.000305 |
| format | Article |
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METHODS AND RESULTS—We identified 3 single-nucleotide polymorphisms in CCNB1 associated with increased restenosis risk in a cohort of 284 patients undergoing coronary angioplasty and stent placement (rs350099TT versus CC+TC; odds ratio [OR], 1.82; 95% confidence interval [CI], 1.09–3.03; P=0.023; rs350104CC versus CT+TT; OR, 1.82; 95% CI, 1.02–3.26; P=0.040; and rs164390GG versus GT+TT; OR, 2.27; 95% CI, 1.33–3.85; P=0.002). These findings were replicated in another cohort study of 715 patients (rs350099TT versus CC+TC; OR, 1.88; 95% CI, 0.92–3.81; P=0.080; rs350104CC versus CT+TT; OR, 2.23; 95% CI, 1.18–4.25; P=0.016; and rs164390GG versus GT+TT; OR, 1.87; 95% CI, 1.03–3.47; P=0.040). Moreover, the haplotype containing all 3 risk alleles is associated with higher CCNB1 mRNA expression in circulating lymphocytes and increased in-stent restenosis risk (OR, 1.43; 95% CI, 1.00–1.823; P=0.039). The risk variants of rs350099, rs350104, and rs164390 are associated with increased reporter gene expression through binding of transcription factors nuclear factor-Y, activator protein 1, and specificity protein 1, respectively.
CONCLUSIONS—Allele-dependent transcriptional regulation of CCNB1 associated with rs350099, rs350104, and rs164390 affects the risk of in-stent restenosis. These findings reveal these common genetic variations as attractive diagnostic tools in risk stratification for restenosis.</description><identifier>ISSN: 1942-325X</identifier><identifier>EISSN: 1942-3268</identifier><identifier>DOI: 10.1161/CIRCGENETICS.113.000305</identifier><identifier>PMID: 24395923</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Alleles ; CCAAT-Binding Factor - genetics ; CCAAT-Binding Factor - metabolism ; Cohort Studies ; Coronary Angiography ; Coronary Restenosis - etiology ; Coronary Restenosis - genetics ; Coronary Restenosis - mortality ; Cyclin B1 - genetics ; Cyclin B1 - metabolism ; Drug-Eluting Stents ; Genotype ; Haplotypes ; Humans ; Kaplan-Meier Estimate ; Odds Ratio ; Polymorphism, Single Nucleotide ; Proportional Hazards Models ; Risk Factors ; RNA, Messenger - metabolism ; Sp1 Transcription Factor - genetics ; Sp1 Transcription Factor - metabolism ; Transcription Factor AP-1 - genetics ; Transcription Factor AP-1 - metabolism ; Transcription, Genetic</subject><ispartof>Circulation. Cardiovascular genetics, 2014-02, Vol.7 (1), p.59-70</ispartof><rights>2014 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4145-6b75599d0513b06c92e8268c4f55f938dcaf1fea6e793eaa30bba3e7862dff2b3</citedby><cites>FETCH-LOGICAL-c4145-6b75599d0513b06c92e8268c4f55f938dcaf1fea6e793eaa30bba3e7862dff2b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3688,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24395923$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Silvestre-Roig, Carlos</creatorcontrib><creatorcontrib>Fernández, Patricia</creatorcontrib><creatorcontrib>Mansego, María L</creatorcontrib><creatorcontrib>van Tiel, Claudia M</creatorcontrib><creatorcontrib>Viana, Rosa</creatorcontrib><creatorcontrib>Anselmi, Chiara Viviani</creatorcontrib><creatorcontrib>Condorelli, Gianluigi</creatorcontrib><creatorcontrib>de Winter, Robbert J</creatorcontrib><creatorcontrib>Martín-Fuentes, Paula</creatorcontrib><creatorcontrib>Solanas-Barca, María</creatorcontrib><creatorcontrib>Civeira, Fernando</creatorcontrib><creatorcontrib>Focaccio, Amelia</creatorcontrib><creatorcontrib>de Vries, Carlie J.M</creatorcontrib><creatorcontrib>Chaves, Felipe Javier</creatorcontrib><creatorcontrib>Andrés, Vicente</creatorcontrib><title>Genetic Variants in CCNB1 Associated With Differential Gene Transcription and Risk of Coronary In-Stent Restenosis</title><title>Circulation. Cardiovascular genetics</title><addtitle>Circ Cardiovasc Genet</addtitle><description>BACKGROUND—The development of diagnostic tools to assess restenosis risk after stent deployment may enable the intervention to be tailored to the individual patient, for example, by targeting the use of drug-eluting stent to high-risk patients, with the goal of improving safety and reducing costs. The CCNB1 gene (encoding cyclin B1) positively regulates cell proliferation, a key component of in-stent restenosis. Therefore, we hypothesized that single-nucleotide polymorphisms in CCNB1 may serve as useful tools in risk stratification for in-stent restenosis.
METHODS AND RESULTS—We identified 3 single-nucleotide polymorphisms in CCNB1 associated with increased restenosis risk in a cohort of 284 patients undergoing coronary angioplasty and stent placement (rs350099TT versus CC+TC; odds ratio [OR], 1.82; 95% confidence interval [CI], 1.09–3.03; P=0.023; rs350104CC versus CT+TT; OR, 1.82; 95% CI, 1.02–3.26; P=0.040; and rs164390GG versus GT+TT; OR, 2.27; 95% CI, 1.33–3.85; P=0.002). These findings were replicated in another cohort study of 715 patients (rs350099TT versus CC+TC; OR, 1.88; 95% CI, 0.92–3.81; P=0.080; rs350104CC versus CT+TT; OR, 2.23; 95% CI, 1.18–4.25; P=0.016; and rs164390GG versus GT+TT; OR, 1.87; 95% CI, 1.03–3.47; P=0.040). Moreover, the haplotype containing all 3 risk alleles is associated with higher CCNB1 mRNA expression in circulating lymphocytes and increased in-stent restenosis risk (OR, 1.43; 95% CI, 1.00–1.823; P=0.039). The risk variants of rs350099, rs350104, and rs164390 are associated with increased reporter gene expression through binding of transcription factors nuclear factor-Y, activator protein 1, and specificity protein 1, respectively.
CONCLUSIONS—Allele-dependent transcriptional regulation of CCNB1 associated with rs350099, rs350104, and rs164390 affects the risk of in-stent restenosis. These findings reveal these common genetic variations as attractive diagnostic tools in risk stratification for restenosis.</description><subject>Alleles</subject><subject>CCAAT-Binding Factor - genetics</subject><subject>CCAAT-Binding Factor - metabolism</subject><subject>Cohort Studies</subject><subject>Coronary Angiography</subject><subject>Coronary Restenosis - etiology</subject><subject>Coronary Restenosis - genetics</subject><subject>Coronary Restenosis - mortality</subject><subject>Cyclin B1 - genetics</subject><subject>Cyclin B1 - metabolism</subject><subject>Drug-Eluting Stents</subject><subject>Genotype</subject><subject>Haplotypes</subject><subject>Humans</subject><subject>Kaplan-Meier Estimate</subject><subject>Odds Ratio</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Proportional Hazards Models</subject><subject>Risk Factors</subject><subject>RNA, Messenger - metabolism</subject><subject>Sp1 Transcription Factor - genetics</subject><subject>Sp1 Transcription Factor - metabolism</subject><subject>Transcription Factor AP-1 - genetics</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Transcription, Genetic</subject><issn>1942-325X</issn><issn>1942-3268</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkElPwzAQhS0EYv8L4COXgB3HWcQJQimVKpBKWW6R44xVQ2oX21XFv8dVAXHj9Eaj92b5EDql5JzSnF7Uo0k9HNwPpqP6MXbYOSGEEb6F9mmVpQlL83L7t-ave-jA-zdC8oyxfBftpRmreJWyfeSGYCBoiZ-F08IEj7XBdX1_TfGV91ZqEaDDLzrM8I1WChyYoEWP1zE8dcJ46fQiaGuwMB2eaP-OrcK1ddYI94lHJnkMMYMn4KNar_0R2lGi93D8rYfo6XYwre-S8cNwVF-NE5nRjCd5W3BeVR3hlLUkl1UKZXxLZopzVbGyk0JRBSKHomIgBCNtKxgUZZ52SqUtO0Rnm7kLZz-WcX0z115C3wsDdukbyiOQsshSEq3Fxiqd9d6BahZOz-P9DSXNGnjzF3jssGYDPCZPvpcs2zl0v7kfwtFwuTGsbB_A-fd-uQLXzED0Yfbv-C9g_JC2</recordid><startdate>201402</startdate><enddate>201402</enddate><creator>Silvestre-Roig, Carlos</creator><creator>Fernández, Patricia</creator><creator>Mansego, María L</creator><creator>van Tiel, Claudia M</creator><creator>Viana, Rosa</creator><creator>Anselmi, Chiara Viviani</creator><creator>Condorelli, Gianluigi</creator><creator>de Winter, Robbert J</creator><creator>Martín-Fuentes, Paula</creator><creator>Solanas-Barca, María</creator><creator>Civeira, Fernando</creator><creator>Focaccio, Amelia</creator><creator>de Vries, Carlie J.M</creator><creator>Chaves, Felipe Javier</creator><creator>Andrés, Vicente</creator><general>American Heart Association, Inc</general><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>201402</creationdate><title>Genetic Variants in CCNB1 Associated With Differential Gene Transcription and Risk of Coronary In-Stent Restenosis</title><author>Silvestre-Roig, Carlos ; Fernández, Patricia ; Mansego, María L ; van Tiel, Claudia M ; Viana, Rosa ; Anselmi, Chiara Viviani ; Condorelli, Gianluigi ; de Winter, Robbert J ; Martín-Fuentes, Paula ; Solanas-Barca, María ; Civeira, Fernando ; Focaccio, Amelia ; de Vries, Carlie J.M ; Chaves, Felipe Javier ; Andrés, Vicente</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4145-6b75599d0513b06c92e8268c4f55f938dcaf1fea6e793eaa30bba3e7862dff2b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Alleles</topic><topic>CCAAT-Binding Factor - genetics</topic><topic>CCAAT-Binding Factor - metabolism</topic><topic>Cohort Studies</topic><topic>Coronary Angiography</topic><topic>Coronary Restenosis - etiology</topic><topic>Coronary Restenosis - genetics</topic><topic>Coronary Restenosis - mortality</topic><topic>Cyclin B1 - genetics</topic><topic>Cyclin B1 - metabolism</topic><topic>Drug-Eluting Stents</topic><topic>Genotype</topic><topic>Haplotypes</topic><topic>Humans</topic><topic>Kaplan-Meier Estimate</topic><topic>Odds Ratio</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Proportional Hazards Models</topic><topic>Risk Factors</topic><topic>RNA, Messenger - metabolism</topic><topic>Sp1 Transcription Factor - genetics</topic><topic>Sp1 Transcription Factor - metabolism</topic><topic>Transcription Factor AP-1 - genetics</topic><topic>Transcription Factor AP-1 - metabolism</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Silvestre-Roig, Carlos</creatorcontrib><creatorcontrib>Fernández, Patricia</creatorcontrib><creatorcontrib>Mansego, María L</creatorcontrib><creatorcontrib>van Tiel, Claudia M</creatorcontrib><creatorcontrib>Viana, Rosa</creatorcontrib><creatorcontrib>Anselmi, Chiara Viviani</creatorcontrib><creatorcontrib>Condorelli, Gianluigi</creatorcontrib><creatorcontrib>de Winter, Robbert J</creatorcontrib><creatorcontrib>Martín-Fuentes, Paula</creatorcontrib><creatorcontrib>Solanas-Barca, María</creatorcontrib><creatorcontrib>Civeira, Fernando</creatorcontrib><creatorcontrib>Focaccio, Amelia</creatorcontrib><creatorcontrib>de Vries, Carlie J.M</creatorcontrib><creatorcontrib>Chaves, Felipe Javier</creatorcontrib><creatorcontrib>Andrés, Vicente</creatorcontrib><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>Circulation. Cardiovascular genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Silvestre-Roig, Carlos</au><au>Fernández, Patricia</au><au>Mansego, María L</au><au>van Tiel, Claudia M</au><au>Viana, Rosa</au><au>Anselmi, Chiara Viviani</au><au>Condorelli, Gianluigi</au><au>de Winter, Robbert J</au><au>Martín-Fuentes, Paula</au><au>Solanas-Barca, María</au><au>Civeira, Fernando</au><au>Focaccio, Amelia</au><au>de Vries, Carlie J.M</au><au>Chaves, Felipe Javier</au><au>Andrés, Vicente</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic Variants in CCNB1 Associated With Differential Gene Transcription and Risk of Coronary In-Stent Restenosis</atitle><jtitle>Circulation. Cardiovascular genetics</jtitle><addtitle>Circ Cardiovasc Genet</addtitle><date>2014-02</date><risdate>2014</risdate><volume>7</volume><issue>1</issue><spage>59</spage><epage>70</epage><pages>59-70</pages><issn>1942-325X</issn><eissn>1942-3268</eissn><abstract>BACKGROUND—The development of diagnostic tools to assess restenosis risk after stent deployment may enable the intervention to be tailored to the individual patient, for example, by targeting the use of drug-eluting stent to high-risk patients, with the goal of improving safety and reducing costs. The CCNB1 gene (encoding cyclin B1) positively regulates cell proliferation, a key component of in-stent restenosis. Therefore, we hypothesized that single-nucleotide polymorphisms in CCNB1 may serve as useful tools in risk stratification for in-stent restenosis.
METHODS AND RESULTS—We identified 3 single-nucleotide polymorphisms in CCNB1 associated with increased restenosis risk in a cohort of 284 patients undergoing coronary angioplasty and stent placement (rs350099TT versus CC+TC; odds ratio [OR], 1.82; 95% confidence interval [CI], 1.09–3.03; P=0.023; rs350104CC versus CT+TT; OR, 1.82; 95% CI, 1.02–3.26; P=0.040; and rs164390GG versus GT+TT; OR, 2.27; 95% CI, 1.33–3.85; P=0.002). These findings were replicated in another cohort study of 715 patients (rs350099TT versus CC+TC; OR, 1.88; 95% CI, 0.92–3.81; P=0.080; rs350104CC versus CT+TT; OR, 2.23; 95% CI, 1.18–4.25; P=0.016; and rs164390GG versus GT+TT; OR, 1.87; 95% CI, 1.03–3.47; P=0.040). Moreover, the haplotype containing all 3 risk alleles is associated with higher CCNB1 mRNA expression in circulating lymphocytes and increased in-stent restenosis risk (OR, 1.43; 95% CI, 1.00–1.823; P=0.039). The risk variants of rs350099, rs350104, and rs164390 are associated with increased reporter gene expression through binding of transcription factors nuclear factor-Y, activator protein 1, and specificity protein 1, respectively.
CONCLUSIONS—Allele-dependent transcriptional regulation of CCNB1 associated with rs350099, rs350104, and rs164390 affects the risk of in-stent restenosis. These findings reveal these common genetic variations as attractive diagnostic tools in risk stratification for restenosis.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>24395923</pmid><doi>10.1161/CIRCGENETICS.113.000305</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation. Cardiovascular genetics, 2014-02, Vol.7 (1), p.59-70 |
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| source | MEDLINE; American Heart Association Journals |
| subjects | Alleles CCAAT-Binding Factor - genetics CCAAT-Binding Factor - metabolism Cohort Studies Coronary Angiography Coronary Restenosis - etiology Coronary Restenosis - genetics Coronary Restenosis - mortality Cyclin B1 - genetics Cyclin B1 - metabolism Drug-Eluting Stents Genotype Haplotypes Humans Kaplan-Meier Estimate Odds Ratio Polymorphism, Single Nucleotide Proportional Hazards Models Risk Factors RNA, Messenger - metabolism Sp1 Transcription Factor - genetics Sp1 Transcription Factor - metabolism Transcription Factor AP-1 - genetics Transcription Factor AP-1 - metabolism Transcription, Genetic |
| title | Genetic Variants in CCNB1 Associated With Differential Gene Transcription and Risk of Coronary In-Stent Restenosis |
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