A multigene test for the risk of sporadic breast carcinoma
BACKGROUND Although the identification of the BRCA1 and BRCA2 genes have been of great interest, these genes account for less than 5% of all breast carcinoma cases. The remaining cases are sporadic. Reanalysis of a large twin study suggested that genetic factors may play a significant role in sporad...
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| creator | Comings, David E. Gade‐Andavolu, Radhika Cone, Lawrence A. Muhleman, Donn MacMurray, James P. |
| description | BACKGROUND
Although the identification of the BRCA1 and BRCA2 genes have been of great interest, these genes account for less than 5% of all breast carcinoma cases. The remaining cases are sporadic. Reanalysis of a large twin study suggested that genetic factors may play a significant role in sporadic breast and other carcinomas. Sporadic breast carcinoma is polygenically inherited. Multiple genes are likely to have an additive effect, each gene accounting for a fraction of the variance. One factor that may have an impact on the development of hormonally responsive breast tumors is the duration of exposure of the breast to estrogen. Therefore, one of the demographic risk factors for breast carcinoma is an early age of onset of menarche. The current study was based on the hypothesis that genes that play a role in demographic risk factors may be breast carcinoma risk genes in their own right. The authors hypothesized that six genes relevant to the timing of the onset of menarche and related risk factors might be candidate genes for breast carcinoma. These were the leptin gene (LEP), the leptin receptor gene (LEPR), the catechol‐0‐methyltransferase gene (COMT), the dopamine D2 receptor gene (DRD2), the estrogen 1 receptor gene (ESR1), and the androgen receptor gene (AR).
METHODS
The authors examined 67 women with postmenopausal sporadic breast carcinoma and 145 gender and race‐matched controls.
RESULTS
Five of these genes accounted for a significant percent of the variance (r2) of breast carcinoma. The following r2 and P values were calculated: LEP: 0.073, P ≤ 0.0001; LEPR: 0.064, P ≤ 0.0002; COMT: 0.073, P ≤ 0.0001; AR: 0.040, P ≤ 0.0035; and DRD2: 0.018, P ≤ 0.05. When evaluated in a multivariate regression analysis, they accounted collectively for 24% of the variance of breast carcinoma (P ≤ 0.0001). These genes accounted for 40% of the variance (P ≤ 0.00001) in a subset of age‐matched cases. Individual gene scores were added to form a breast carcinoma risk score (BCRS) that ranged from 0 to 17. When the BCRS was evaluated in a receiver operator characteristic plot, the area under the curve was 0.80 for the full set and 0.869 for the age‐matched set. The relative breast carcinoma risk for the different BCRS scores ranged from 0.10 to 11.9.
CONCLUSIONS
These results demonstrate a potentially powerful method of evaluating the additive effect of multiple breast carcinoma risk genes to form a potentially clinically useful assessment of women's risk for sporadi |
| doi_str_mv | 10.1002/cncr.11340 |
| format | Article |
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Although the identification of the BRCA1 and BRCA2 genes have been of great interest, these genes account for less than 5% of all breast carcinoma cases. The remaining cases are sporadic. Reanalysis of a large twin study suggested that genetic factors may play a significant role in sporadic breast and other carcinomas. Sporadic breast carcinoma is polygenically inherited. Multiple genes are likely to have an additive effect, each gene accounting for a fraction of the variance. One factor that may have an impact on the development of hormonally responsive breast tumors is the duration of exposure of the breast to estrogen. Therefore, one of the demographic risk factors for breast carcinoma is an early age of onset of menarche. The current study was based on the hypothesis that genes that play a role in demographic risk factors may be breast carcinoma risk genes in their own right. The authors hypothesized that six genes relevant to the timing of the onset of menarche and related risk factors might be candidate genes for breast carcinoma. These were the leptin gene (LEP), the leptin receptor gene (LEPR), the catechol‐0‐methyltransferase gene (COMT), the dopamine D2 receptor gene (DRD2), the estrogen 1 receptor gene (ESR1), and the androgen receptor gene (AR).
METHODS
The authors examined 67 women with postmenopausal sporadic breast carcinoma and 145 gender and race‐matched controls.
RESULTS
Five of these genes accounted for a significant percent of the variance (r2) of breast carcinoma. The following r2 and P values were calculated: LEP: 0.073, P ≤ 0.0001; LEPR: 0.064, P ≤ 0.0002; COMT: 0.073, P ≤ 0.0001; AR: 0.040, P ≤ 0.0035; and DRD2: 0.018, P ≤ 0.05. When evaluated in a multivariate regression analysis, they accounted collectively for 24% of the variance of breast carcinoma (P ≤ 0.0001). These genes accounted for 40% of the variance (P ≤ 0.00001) in a subset of age‐matched cases. Individual gene scores were added to form a breast carcinoma risk score (BCRS) that ranged from 0 to 17. When the BCRS was evaluated in a receiver operator characteristic plot, the area under the curve was 0.80 for the full set and 0.869 for the age‐matched set. The relative breast carcinoma risk for the different BCRS scores ranged from 0.10 to 11.9.
CONCLUSIONS
These results demonstrate a potentially powerful method of evaluating the additive effect of multiple breast carcinoma risk genes to form a potentially clinically useful assessment of women's risk for sporadic breast carcinoma. Cancer 2003;97:2160–70. © 2003 American Cancer Society.
DOI 10.1002/cncr.11340
Genes that play a role in risk factors for breast carcinoma, such as the age of onset of menarche, might be breast carcinoma risk genes. Using this hypothesis, the authors evaluated the additive effect of six genes (leptin, leptin receptor, catecol‐o‐methyltransferase, dopamine D2 receptor, estrogen receptor, and androgen receptor) in 67 women with sporadic breast carcinoma and in 145 sex and gender‐matched controls. An additive breast carcinoma risk score also was evaluated by receiver operator characteristic plots.</description><identifier>ISSN: 0008-543X</identifier><identifier>EISSN: 1097-0142</identifier><identifier>DOI: 10.1002/cncr.11340</identifier><identifier>PMID: 12712467</identifier><identifier>CODEN: CANCAR</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Age Distribution ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Biomarkers, Tumor - genetics ; breast ; Breast Neoplasms - etiology ; Breast Neoplasms - genetics ; carcinoma ; Case-Control Studies ; Catechol O-Methyltransferase - genetics ; Female ; Genetic Predisposition to Disease ; Genotype ; Gynecology. Andrology. Obstetrics ; Humans ; Leptin - genetics ; Mammary gland diseases ; Medical sciences ; menarche ; Middle Aged ; Neoplasm Proteins - genetics ; polygenic ; Polymorphism, Genetic ; Receptors, Androgen - genetics ; Receptors, Cell Surface - genetics ; Receptors, Dopamine D2 - genetics ; Receptors, Estrogen - genetics ; Receptors, Leptin ; risk ; Risk Factors ; ROC Curve ; Sensitivity and Specificity ; Tumors</subject><ispartof>Cancer, 2003-05, Vol.97 (9), p.2160-2170</ispartof><rights>Copyright © 2003 American Cancer Society</rights><rights>2003 INIST-CNRS</rights><rights>Copyright 2003 American Cancer Society.DOI 10.1002/cncr.11340</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4230-739fe5284356873e9693396b3a3d2f7ac40f8a48a8d11d9e59fff5519ad5d00e3</citedby><cites>FETCH-LOGICAL-c4230-739fe5284356873e9693396b3a3d2f7ac40f8a48a8d11d9e59fff5519ad5d00e3</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%2Fcncr.11340$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fcncr.11340$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,1432,27923,27924,45573,45574,46408,46832</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14708051$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12712467$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Comings, David E.</creatorcontrib><creatorcontrib>Gade‐Andavolu, Radhika</creatorcontrib><creatorcontrib>Cone, Lawrence A.</creatorcontrib><creatorcontrib>Muhleman, Donn</creatorcontrib><creatorcontrib>MacMurray, James P.</creatorcontrib><title>A multigene test for the risk of sporadic breast carcinoma</title><title>Cancer</title><addtitle>Cancer</addtitle><description>BACKGROUND
Although the identification of the BRCA1 and BRCA2 genes have been of great interest, these genes account for less than 5% of all breast carcinoma cases. The remaining cases are sporadic. Reanalysis of a large twin study suggested that genetic factors may play a significant role in sporadic breast and other carcinomas. Sporadic breast carcinoma is polygenically inherited. Multiple genes are likely to have an additive effect, each gene accounting for a fraction of the variance. One factor that may have an impact on the development of hormonally responsive breast tumors is the duration of exposure of the breast to estrogen. Therefore, one of the demographic risk factors for breast carcinoma is an early age of onset of menarche. The current study was based on the hypothesis that genes that play a role in demographic risk factors may be breast carcinoma risk genes in their own right. The authors hypothesized that six genes relevant to the timing of the onset of menarche and related risk factors might be candidate genes for breast carcinoma. These were the leptin gene (LEP), the leptin receptor gene (LEPR), the catechol‐0‐methyltransferase gene (COMT), the dopamine D2 receptor gene (DRD2), the estrogen 1 receptor gene (ESR1), and the androgen receptor gene (AR).
METHODS
The authors examined 67 women with postmenopausal sporadic breast carcinoma and 145 gender and race‐matched controls.
RESULTS
Five of these genes accounted for a significant percent of the variance (r2) of breast carcinoma. The following r2 and P values were calculated: LEP: 0.073, P ≤ 0.0001; LEPR: 0.064, P ≤ 0.0002; COMT: 0.073, P ≤ 0.0001; AR: 0.040, P ≤ 0.0035; and DRD2: 0.018, P ≤ 0.05. When evaluated in a multivariate regression analysis, they accounted collectively for 24% of the variance of breast carcinoma (P ≤ 0.0001). These genes accounted for 40% of the variance (P ≤ 0.00001) in a subset of age‐matched cases. Individual gene scores were added to form a breast carcinoma risk score (BCRS) that ranged from 0 to 17. When the BCRS was evaluated in a receiver operator characteristic plot, the area under the curve was 0.80 for the full set and 0.869 for the age‐matched set. The relative breast carcinoma risk for the different BCRS scores ranged from 0.10 to 11.9.
CONCLUSIONS
These results demonstrate a potentially powerful method of evaluating the additive effect of multiple breast carcinoma risk genes to form a potentially clinically useful assessment of women's risk for sporadic breast carcinoma. Cancer 2003;97:2160–70. © 2003 American Cancer Society.
DOI 10.1002/cncr.11340
Genes that play a role in risk factors for breast carcinoma, such as the age of onset of menarche, might be breast carcinoma risk genes. Using this hypothesis, the authors evaluated the additive effect of six genes (leptin, leptin receptor, catecol‐o‐methyltransferase, dopamine D2 receptor, estrogen receptor, and androgen receptor) in 67 women with sporadic breast carcinoma and in 145 sex and gender‐matched controls. An additive breast carcinoma risk score also was evaluated by receiver operator characteristic plots.</description><subject>Adult</subject><subject>Age Distribution</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - genetics</subject><subject>breast</subject><subject>Breast Neoplasms - etiology</subject><subject>Breast Neoplasms - genetics</subject><subject>carcinoma</subject><subject>Case-Control Studies</subject><subject>Catechol O-Methyltransferase - genetics</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Leptin - genetics</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>menarche</subject><subject>Middle Aged</subject><subject>Neoplasm Proteins - genetics</subject><subject>polygenic</subject><subject>Polymorphism, Genetic</subject><subject>Receptors, Androgen - genetics</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Dopamine D2 - genetics</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Leptin</subject><subject>risk</subject><subject>Risk Factors</subject><subject>ROC Curve</subject><subject>Sensitivity and Specificity</subject><subject>Tumors</subject><issn>0008-543X</issn><issn>1097-0142</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90EtLw0AQB_BFFFurFz-A7EUFIXX2lc16K8EXFAVR8Ba2m12N5lF3E6Tf3tQGeutpGObHzPBH6JTAlADQa1MbPyWEcdhDYwJKRkA43UdjAEgiwdn7CB2F8NW3kgp2iEaESkJ5LMfoZoarrmyLD1tb3NrQYtd43H5a7IvwjRuHw7LxOi8MXnir-7nR3hR1U-ljdOB0GezJUCfo7e72NX2I5s_3j-lsHhlOGUSSKWcFTTgTcSKZVbFiTMULpllOndSGg0s0T3SSE5IrK5RzTgiidC5yAMsm6HKzd-mbn65_MauKYGxZ6to2Xcik4IkUjKpeXuyWjAogIu7h1QYa34TgrcuWvqi0X2UEsnWm2TrT7D_THp8NW7tFZfMtHULswfkAdDC6dF7XpghbxyUkIEjvyMb9FqVd7TiZpU_py-b4HyxIjEQ</recordid><startdate>20030501</startdate><enddate>20030501</enddate><creator>Comings, David E.</creator><creator>Gade‐Andavolu, Radhika</creator><creator>Cone, Lawrence A.</creator><creator>Muhleman, Donn</creator><creator>MacMurray, James P.</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>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20030501</creationdate><title>A multigene test for the risk of sporadic breast carcinoma</title><author>Comings, David E. ; Gade‐Andavolu, Radhika ; Cone, Lawrence A. ; Muhleman, Donn ; MacMurray, James P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4230-739fe5284356873e9693396b3a3d2f7ac40f8a48a8d11d9e59fff5519ad5d00e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adult</topic><topic>Age Distribution</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - genetics</topic><topic>breast</topic><topic>Breast Neoplasms - etiology</topic><topic>Breast Neoplasms - genetics</topic><topic>carcinoma</topic><topic>Case-Control Studies</topic><topic>Catechol O-Methyltransferase - genetics</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Leptin - genetics</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>menarche</topic><topic>Middle Aged</topic><topic>Neoplasm Proteins - genetics</topic><topic>polygenic</topic><topic>Polymorphism, Genetic</topic><topic>Receptors, Androgen - genetics</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Dopamine D2 - genetics</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, Leptin</topic><topic>risk</topic><topic>Risk Factors</topic><topic>ROC Curve</topic><topic>Sensitivity and Specificity</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Comings, David E.</creatorcontrib><creatorcontrib>Gade‐Andavolu, Radhika</creatorcontrib><creatorcontrib>Cone, Lawrence A.</creatorcontrib><creatorcontrib>Muhleman, Donn</creatorcontrib><creatorcontrib>MacMurray, James P.</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><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Comings, David E.</au><au>Gade‐Andavolu, Radhika</au><au>Cone, Lawrence A.</au><au>Muhleman, Donn</au><au>MacMurray, James P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A multigene test for the risk of sporadic breast carcinoma</atitle><jtitle>Cancer</jtitle><addtitle>Cancer</addtitle><date>2003-05-01</date><risdate>2003</risdate><volume>97</volume><issue>9</issue><spage>2160</spage><epage>2170</epage><pages>2160-2170</pages><issn>0008-543X</issn><eissn>1097-0142</eissn><coden>CANCAR</coden><abstract>BACKGROUND
Although the identification of the BRCA1 and BRCA2 genes have been of great interest, these genes account for less than 5% of all breast carcinoma cases. The remaining cases are sporadic. Reanalysis of a large twin study suggested that genetic factors may play a significant role in sporadic breast and other carcinomas. Sporadic breast carcinoma is polygenically inherited. Multiple genes are likely to have an additive effect, each gene accounting for a fraction of the variance. One factor that may have an impact on the development of hormonally responsive breast tumors is the duration of exposure of the breast to estrogen. Therefore, one of the demographic risk factors for breast carcinoma is an early age of onset of menarche. The current study was based on the hypothesis that genes that play a role in demographic risk factors may be breast carcinoma risk genes in their own right. The authors hypothesized that six genes relevant to the timing of the onset of menarche and related risk factors might be candidate genes for breast carcinoma. These were the leptin gene (LEP), the leptin receptor gene (LEPR), the catechol‐0‐methyltransferase gene (COMT), the dopamine D2 receptor gene (DRD2), the estrogen 1 receptor gene (ESR1), and the androgen receptor gene (AR).
METHODS
The authors examined 67 women with postmenopausal sporadic breast carcinoma and 145 gender and race‐matched controls.
RESULTS
Five of these genes accounted for a significant percent of the variance (r2) of breast carcinoma. The following r2 and P values were calculated: LEP: 0.073, P ≤ 0.0001; LEPR: 0.064, P ≤ 0.0002; COMT: 0.073, P ≤ 0.0001; AR: 0.040, P ≤ 0.0035; and DRD2: 0.018, P ≤ 0.05. When evaluated in a multivariate regression analysis, they accounted collectively for 24% of the variance of breast carcinoma (P ≤ 0.0001). These genes accounted for 40% of the variance (P ≤ 0.00001) in a subset of age‐matched cases. Individual gene scores were added to form a breast carcinoma risk score (BCRS) that ranged from 0 to 17. When the BCRS was evaluated in a receiver operator characteristic plot, the area under the curve was 0.80 for the full set and 0.869 for the age‐matched set. The relative breast carcinoma risk for the different BCRS scores ranged from 0.10 to 11.9.
CONCLUSIONS
These results demonstrate a potentially powerful method of evaluating the additive effect of multiple breast carcinoma risk genes to form a potentially clinically useful assessment of women's risk for sporadic breast carcinoma. Cancer 2003;97:2160–70. © 2003 American Cancer Society.
DOI 10.1002/cncr.11340
Genes that play a role in risk factors for breast carcinoma, such as the age of onset of menarche, might be breast carcinoma risk genes. Using this hypothesis, the authors evaluated the additive effect of six genes (leptin, leptin receptor, catecol‐o‐methyltransferase, dopamine D2 receptor, estrogen receptor, and androgen receptor) in 67 women with sporadic breast carcinoma and in 145 sex and gender‐matched controls. An additive breast carcinoma risk score also was evaluated by receiver operator characteristic plots.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>12712467</pmid><doi>10.1002/cncr.11340</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Age Distribution Aged Aged, 80 and over Biological and medical sciences Biomarkers, Tumor - genetics breast Breast Neoplasms - etiology Breast Neoplasms - genetics carcinoma Case-Control Studies Catechol O-Methyltransferase - genetics Female Genetic Predisposition to Disease Genotype Gynecology. Andrology. Obstetrics Humans Leptin - genetics Mammary gland diseases Medical sciences menarche Middle Aged Neoplasm Proteins - genetics polygenic Polymorphism, Genetic Receptors, Androgen - genetics Receptors, Cell Surface - genetics Receptors, Dopamine D2 - genetics Receptors, Estrogen - genetics Receptors, Leptin risk Risk Factors ROC Curve Sensitivity and Specificity Tumors |
| title | A multigene test for the risk of sporadic breast carcinoma |
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