Evidence for SMAD3 as a modifier of breast cancer risk in BRCA2mutation carriers
Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate gene...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Walker, Logan C [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2010 |
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| Anmerkung: |
© Walker et al.; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
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| Übergeordnetes Werk: |
Enthalten in: Breast cancer research - London : BioMed Central, 1999, 12(2010), 6 vom: 29. Nov. |
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| Übergeordnetes Werk: |
volume:12 ; year:2010 ; number:6 ; day:29 ; month:11 |
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| DOI / URN: |
10.1186/bcr2785 |
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| Katalog-ID: |
SPR029940982 |
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| 245 | 1 | 0 | |a Evidence for SMAD3 as a modifier of breast cancer risk in BRCA2mutation carriers |
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| 520 | |a Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate genes derived through a novel approach that analysed gene expression differences to prioritise candidate modifier genes for association studies. Methods We successfully genotyped 24 SNPs in a cohort of up to 4,724 BRCA1 and 2,693 BRCA2 female mutation carriers from 15 study groups and assessed whether these variants were associated with risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Results SNPs in five of the 14 candidate genes showed evidence of association with breast cancer risk for BRCA1 or BRCA2 carriers (P < 0.05). Notably, the minor alleles of two SNPs (rs7166081 and rs3825977) in high linkage disequilibrium (r2 = 0.77), located at the SMAD3 locus (15q22), were each associated with increased breast cancer risk for BRCA2 mutation carriers (relative risk = 1.25, 95% confidence interval = 1.07 to 1.45, Ptrend = 0.004; and relative risk = 1.20, 95% confidence interval = 1.03 to 1.40, Ptrend = 0.018). Conclusions This study provides evidence that the SMAD3 gene, which encodes a key regulatory protein in the transforming growth factor beta signalling pathway and is known to interact directly with BRCA2, may contribute to increased risk of breast cancer in BRCA2 mutation carriers. This finding suggests that genes with expression associated with BRCA1 and BRCA2 mutation status are enriched for the presence of common genetic modifiers of breast cancer risk in these populations. | ||
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| 700 | 1 | |a Fredericksen, Zachary S |4 aut | |
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| 700 | 1 | |a Hooning, Maartje J |4 aut | |
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10.1186/bcr2785 doi (DE-627)SPR029940982 (SPR)bcr2785-e DE-627 ger DE-627 rakwb eng Walker, Logan C verfasserin aut Evidence for SMAD3 as a modifier of breast cancer risk in BRCA2mutation carriers 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Walker et al.; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate genes derived through a novel approach that analysed gene expression differences to prioritise candidate modifier genes for association studies. Methods We successfully genotyped 24 SNPs in a cohort of up to 4,724 BRCA1 and 2,693 BRCA2 female mutation carriers from 15 study groups and assessed whether these variants were associated with risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Results SNPs in five of the 14 candidate genes showed evidence of association with breast cancer risk for BRCA1 or BRCA2 carriers (P < 0.05). Notably, the minor alleles of two SNPs (rs7166081 and rs3825977) in high linkage disequilibrium (r2 = 0.77), located at the SMAD3 locus (15q22), were each associated with increased breast cancer risk for BRCA2 mutation carriers (relative risk = 1.25, 95% confidence interval = 1.07 to 1.45, Ptrend = 0.004; and relative risk = 1.20, 95% confidence interval = 1.03 to 1.40, Ptrend = 0.018). Conclusions This study provides evidence that the SMAD3 gene, which encodes a key regulatory protein in the transforming growth factor beta signalling pathway and is known to interact directly with BRCA2, may contribute to increased risk of breast cancer in BRCA2 mutation carriers. This finding suggests that genes with expression associated with BRCA1 and BRCA2 mutation status are enriched for the presence of common genetic modifiers of breast cancer risk in these populations. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Genetic Modifier (dpeaa)DE-He213 Mutation Carrier (dpeaa)DE-He213 BRCA2 Mutation (dpeaa)DE-He213 Fredericksen, Zachary S aut Wang, Xianshu aut Tarrell, Robert aut Pankratz, Vernon S aut Lindor, Noralane M aut Beesley, Jonathan aut Healey, Sue aut Chen, Xiaoqing aut Stoppa-Lyonnet, Dominique aut Tirapo, Carole aut Giraud, Sophie aut Mazoyer, Sylvie aut Muller, Danièle aut Fricker, Jean-Pierre aut Delnatte, Capucine aut Schmutzler, Rita K aut Wappenschmidt, Barbara aut Engel, Christoph aut Schönbuchner, Ines aut Deissler, Helmut aut Meindl, Alfons aut Hogervorst, Frans B aut Verheus, Martijn aut Hooning, Maartje J aut van den Ouweland, Ans MW aut Nelen, Marcel R aut Ausems, Margreet GEM aut Aalfs, Cora M aut van Asperen, Christi J aut Devilee, Peter aut Gerrits, Monique M aut Waisfisz, Quinten aut Szabo, Csilla I aut Easton, Douglas F aut Peock, Susan aut Cook, Margaret aut Oliver, Clare T aut Frost, Debra aut Harrington, Patricia aut Evans, D Gareth aut Lalloo, Fiona aut Eeles, Ros aut Izatt, Louise aut Chu, Carol aut Davidson, Rosemarie aut Eccles, Diana aut Ong, Kai-Ren aut Cook, Jackie aut Rebbeck, Tim aut Nathanson, Katherine L aut Domchek, Susan M aut Singer, Christian F aut Gschwantler-Kaulich, Daphne aut Dressler, Anne-Catharina aut Pfeiler, Georg aut Godwin, Andrew K aut Heikkinen, Tuomas aut Nevanlinna, Heli aut Agnarsson, Bjarni A aut Caligo, Maria Adelaide aut Olsson, Håkan aut Kristoffersson, Ulf aut Liljegren, Annelie aut Arver, Brita aut Karlsson, Per aut Melin, Beatrice aut Sinilnikova, Olga M aut McGuffog, Lesley aut Antoniou, Antonis C aut Chenevix-Trench, Georgia aut Spurdle, Amanda B aut Couch, Fergus J aut Enthalten in Breast cancer research London : BioMed Central, 1999 12(2010), 6 vom: 29. Nov. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:12 year:2010 number:6 day:29 month:11 https://dx.doi.org/10.1186/bcr2785 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2010 6 29 11 |
| spelling |
10.1186/bcr2785 doi (DE-627)SPR029940982 (SPR)bcr2785-e DE-627 ger DE-627 rakwb eng Walker, Logan C verfasserin aut Evidence for SMAD3 as a modifier of breast cancer risk in BRCA2mutation carriers 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Walker et al.; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate genes derived through a novel approach that analysed gene expression differences to prioritise candidate modifier genes for association studies. Methods We successfully genotyped 24 SNPs in a cohort of up to 4,724 BRCA1 and 2,693 BRCA2 female mutation carriers from 15 study groups and assessed whether these variants were associated with risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Results SNPs in five of the 14 candidate genes showed evidence of association with breast cancer risk for BRCA1 or BRCA2 carriers (P < 0.05). Notably, the minor alleles of two SNPs (rs7166081 and rs3825977) in high linkage disequilibrium (r2 = 0.77), located at the SMAD3 locus (15q22), were each associated with increased breast cancer risk for BRCA2 mutation carriers (relative risk = 1.25, 95% confidence interval = 1.07 to 1.45, Ptrend = 0.004; and relative risk = 1.20, 95% confidence interval = 1.03 to 1.40, Ptrend = 0.018). Conclusions This study provides evidence that the SMAD3 gene, which encodes a key regulatory protein in the transforming growth factor beta signalling pathway and is known to interact directly with BRCA2, may contribute to increased risk of breast cancer in BRCA2 mutation carriers. This finding suggests that genes with expression associated with BRCA1 and BRCA2 mutation status are enriched for the presence of common genetic modifiers of breast cancer risk in these populations. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Genetic Modifier (dpeaa)DE-He213 Mutation Carrier (dpeaa)DE-He213 BRCA2 Mutation (dpeaa)DE-He213 Fredericksen, Zachary S aut Wang, Xianshu aut Tarrell, Robert aut Pankratz, Vernon S aut Lindor, Noralane M aut Beesley, Jonathan aut Healey, Sue aut Chen, Xiaoqing aut Stoppa-Lyonnet, Dominique aut Tirapo, Carole aut Giraud, Sophie aut Mazoyer, Sylvie aut Muller, Danièle aut Fricker, Jean-Pierre aut Delnatte, Capucine aut Schmutzler, Rita K aut Wappenschmidt, Barbara aut Engel, Christoph aut Schönbuchner, Ines aut Deissler, Helmut aut Meindl, Alfons aut Hogervorst, Frans B aut Verheus, Martijn aut Hooning, Maartje J aut van den Ouweland, Ans MW aut Nelen, Marcel R aut Ausems, Margreet GEM aut Aalfs, Cora M aut van Asperen, Christi J aut Devilee, Peter aut Gerrits, Monique M aut Waisfisz, Quinten aut Szabo, Csilla I aut Easton, Douglas F aut Peock, Susan aut Cook, Margaret aut Oliver, Clare T aut Frost, Debra aut Harrington, Patricia aut Evans, D Gareth aut Lalloo, Fiona aut Eeles, Ros aut Izatt, Louise aut Chu, Carol aut Davidson, Rosemarie aut Eccles, Diana aut Ong, Kai-Ren aut Cook, Jackie aut Rebbeck, Tim aut Nathanson, Katherine L aut Domchek, Susan M aut Singer, Christian F aut Gschwantler-Kaulich, Daphne aut Dressler, Anne-Catharina aut Pfeiler, Georg aut Godwin, Andrew K aut Heikkinen, Tuomas aut Nevanlinna, Heli aut Agnarsson, Bjarni A aut Caligo, Maria Adelaide aut Olsson, Håkan aut Kristoffersson, Ulf aut Liljegren, Annelie aut Arver, Brita aut Karlsson, Per aut Melin, Beatrice aut Sinilnikova, Olga M aut McGuffog, Lesley aut Antoniou, Antonis C aut Chenevix-Trench, Georgia aut Spurdle, Amanda B aut Couch, Fergus J aut Enthalten in Breast cancer research London : BioMed Central, 1999 12(2010), 6 vom: 29. Nov. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:12 year:2010 number:6 day:29 month:11 https://dx.doi.org/10.1186/bcr2785 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2010 6 29 11 |
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10.1186/bcr2785 doi (DE-627)SPR029940982 (SPR)bcr2785-e DE-627 ger DE-627 rakwb eng Walker, Logan C verfasserin aut Evidence for SMAD3 as a modifier of breast cancer risk in BRCA2mutation carriers 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Walker et al.; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate genes derived through a novel approach that analysed gene expression differences to prioritise candidate modifier genes for association studies. Methods We successfully genotyped 24 SNPs in a cohort of up to 4,724 BRCA1 and 2,693 BRCA2 female mutation carriers from 15 study groups and assessed whether these variants were associated with risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Results SNPs in five of the 14 candidate genes showed evidence of association with breast cancer risk for BRCA1 or BRCA2 carriers (P < 0.05). Notably, the minor alleles of two SNPs (rs7166081 and rs3825977) in high linkage disequilibrium (r2 = 0.77), located at the SMAD3 locus (15q22), were each associated with increased breast cancer risk for BRCA2 mutation carriers (relative risk = 1.25, 95% confidence interval = 1.07 to 1.45, Ptrend = 0.004; and relative risk = 1.20, 95% confidence interval = 1.03 to 1.40, Ptrend = 0.018). Conclusions This study provides evidence that the SMAD3 gene, which encodes a key regulatory protein in the transforming growth factor beta signalling pathway and is known to interact directly with BRCA2, may contribute to increased risk of breast cancer in BRCA2 mutation carriers. This finding suggests that genes with expression associated with BRCA1 and BRCA2 mutation status are enriched for the presence of common genetic modifiers of breast cancer risk in these populations. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Genetic Modifier (dpeaa)DE-He213 Mutation Carrier (dpeaa)DE-He213 BRCA2 Mutation (dpeaa)DE-He213 Fredericksen, Zachary S aut Wang, Xianshu aut Tarrell, Robert aut Pankratz, Vernon S aut Lindor, Noralane M aut Beesley, Jonathan aut Healey, Sue aut Chen, Xiaoqing aut Stoppa-Lyonnet, Dominique aut Tirapo, Carole aut Giraud, Sophie aut Mazoyer, Sylvie aut Muller, Danièle aut Fricker, Jean-Pierre aut Delnatte, Capucine aut Schmutzler, Rita K aut Wappenschmidt, Barbara aut Engel, Christoph aut Schönbuchner, Ines aut Deissler, Helmut aut Meindl, Alfons aut Hogervorst, Frans B aut Verheus, Martijn aut Hooning, Maartje J aut van den Ouweland, Ans MW aut Nelen, Marcel R aut Ausems, Margreet GEM aut Aalfs, Cora M aut van Asperen, Christi J aut Devilee, Peter aut Gerrits, Monique M aut Waisfisz, Quinten aut Szabo, Csilla I aut Easton, Douglas F aut Peock, Susan aut Cook, Margaret aut Oliver, Clare T aut Frost, Debra aut Harrington, Patricia aut Evans, D Gareth aut Lalloo, Fiona aut Eeles, Ros aut Izatt, Louise aut Chu, Carol aut Davidson, Rosemarie aut Eccles, Diana aut Ong, Kai-Ren aut Cook, Jackie aut Rebbeck, Tim aut Nathanson, Katherine L aut Domchek, Susan M aut Singer, Christian F aut Gschwantler-Kaulich, Daphne aut Dressler, Anne-Catharina aut Pfeiler, Georg aut Godwin, Andrew K aut Heikkinen, Tuomas aut Nevanlinna, Heli aut Agnarsson, Bjarni A aut Caligo, Maria Adelaide aut Olsson, Håkan aut Kristoffersson, Ulf aut Liljegren, Annelie aut Arver, Brita aut Karlsson, Per aut Melin, Beatrice aut Sinilnikova, Olga M aut McGuffog, Lesley aut Antoniou, Antonis C aut Chenevix-Trench, Georgia aut Spurdle, Amanda B aut Couch, Fergus J aut Enthalten in Breast cancer research London : BioMed Central, 1999 12(2010), 6 vom: 29. Nov. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:12 year:2010 number:6 day:29 month:11 https://dx.doi.org/10.1186/bcr2785 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2010 6 29 11 |
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10.1186/bcr2785 doi (DE-627)SPR029940982 (SPR)bcr2785-e DE-627 ger DE-627 rakwb eng Walker, Logan C verfasserin aut Evidence for SMAD3 as a modifier of breast cancer risk in BRCA2mutation carriers 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Walker et al.; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate genes derived through a novel approach that analysed gene expression differences to prioritise candidate modifier genes for association studies. Methods We successfully genotyped 24 SNPs in a cohort of up to 4,724 BRCA1 and 2,693 BRCA2 female mutation carriers from 15 study groups and assessed whether these variants were associated with risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Results SNPs in five of the 14 candidate genes showed evidence of association with breast cancer risk for BRCA1 or BRCA2 carriers (P < 0.05). Notably, the minor alleles of two SNPs (rs7166081 and rs3825977) in high linkage disequilibrium (r2 = 0.77), located at the SMAD3 locus (15q22), were each associated with increased breast cancer risk for BRCA2 mutation carriers (relative risk = 1.25, 95% confidence interval = 1.07 to 1.45, Ptrend = 0.004; and relative risk = 1.20, 95% confidence interval = 1.03 to 1.40, Ptrend = 0.018). Conclusions This study provides evidence that the SMAD3 gene, which encodes a key regulatory protein in the transforming growth factor beta signalling pathway and is known to interact directly with BRCA2, may contribute to increased risk of breast cancer in BRCA2 mutation carriers. This finding suggests that genes with expression associated with BRCA1 and BRCA2 mutation status are enriched for the presence of common genetic modifiers of breast cancer risk in these populations. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Genetic Modifier (dpeaa)DE-He213 Mutation Carrier (dpeaa)DE-He213 BRCA2 Mutation (dpeaa)DE-He213 Fredericksen, Zachary S aut Wang, Xianshu aut Tarrell, Robert aut Pankratz, Vernon S aut Lindor, Noralane M aut Beesley, Jonathan aut Healey, Sue aut Chen, Xiaoqing aut Stoppa-Lyonnet, Dominique aut Tirapo, Carole aut Giraud, Sophie aut Mazoyer, Sylvie aut Muller, Danièle aut Fricker, Jean-Pierre aut Delnatte, Capucine aut Schmutzler, Rita K aut Wappenschmidt, Barbara aut Engel, Christoph aut Schönbuchner, Ines aut Deissler, Helmut aut Meindl, Alfons aut Hogervorst, Frans B aut Verheus, Martijn aut Hooning, Maartje J aut van den Ouweland, Ans MW aut Nelen, Marcel R aut Ausems, Margreet GEM aut Aalfs, Cora M aut van Asperen, Christi J aut Devilee, Peter aut Gerrits, Monique M aut Waisfisz, Quinten aut Szabo, Csilla I aut Easton, Douglas F aut Peock, Susan aut Cook, Margaret aut Oliver, Clare T aut Frost, Debra aut Harrington, Patricia aut Evans, D Gareth aut Lalloo, Fiona aut Eeles, Ros aut Izatt, Louise aut Chu, Carol aut Davidson, Rosemarie aut Eccles, Diana aut Ong, Kai-Ren aut Cook, Jackie aut Rebbeck, Tim aut Nathanson, Katherine L aut Domchek, Susan M aut Singer, Christian F aut Gschwantler-Kaulich, Daphne aut Dressler, Anne-Catharina aut Pfeiler, Georg aut Godwin, Andrew K aut Heikkinen, Tuomas aut Nevanlinna, Heli aut Agnarsson, Bjarni A aut Caligo, Maria Adelaide aut Olsson, Håkan aut Kristoffersson, Ulf aut Liljegren, Annelie aut Arver, Brita aut Karlsson, Per aut Melin, Beatrice aut Sinilnikova, Olga M aut McGuffog, Lesley aut Antoniou, Antonis C aut Chenevix-Trench, Georgia aut Spurdle, Amanda B aut Couch, Fergus J aut Enthalten in Breast cancer research London : BioMed Central, 1999 12(2010), 6 vom: 29. Nov. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:12 year:2010 number:6 day:29 month:11 https://dx.doi.org/10.1186/bcr2785 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2010 6 29 11 |
| allfieldsSound |
10.1186/bcr2785 doi (DE-627)SPR029940982 (SPR)bcr2785-e DE-627 ger DE-627 rakwb eng Walker, Logan C verfasserin aut Evidence for SMAD3 as a modifier of breast cancer risk in BRCA2mutation carriers 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Walker et al.; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate genes derived through a novel approach that analysed gene expression differences to prioritise candidate modifier genes for association studies. Methods We successfully genotyped 24 SNPs in a cohort of up to 4,724 BRCA1 and 2,693 BRCA2 female mutation carriers from 15 study groups and assessed whether these variants were associated with risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Results SNPs in five of the 14 candidate genes showed evidence of association with breast cancer risk for BRCA1 or BRCA2 carriers (P < 0.05). Notably, the minor alleles of two SNPs (rs7166081 and rs3825977) in high linkage disequilibrium (r2 = 0.77), located at the SMAD3 locus (15q22), were each associated with increased breast cancer risk for BRCA2 mutation carriers (relative risk = 1.25, 95% confidence interval = 1.07 to 1.45, Ptrend = 0.004; and relative risk = 1.20, 95% confidence interval = 1.03 to 1.40, Ptrend = 0.018). Conclusions This study provides evidence that the SMAD3 gene, which encodes a key regulatory protein in the transforming growth factor beta signalling pathway and is known to interact directly with BRCA2, may contribute to increased risk of breast cancer in BRCA2 mutation carriers. This finding suggests that genes with expression associated with BRCA1 and BRCA2 mutation status are enriched for the presence of common genetic modifiers of breast cancer risk in these populations. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Genetic Modifier (dpeaa)DE-He213 Mutation Carrier (dpeaa)DE-He213 BRCA2 Mutation (dpeaa)DE-He213 Fredericksen, Zachary S aut Wang, Xianshu aut Tarrell, Robert aut Pankratz, Vernon S aut Lindor, Noralane M aut Beesley, Jonathan aut Healey, Sue aut Chen, Xiaoqing aut Stoppa-Lyonnet, Dominique aut Tirapo, Carole aut Giraud, Sophie aut Mazoyer, Sylvie aut Muller, Danièle aut Fricker, Jean-Pierre aut Delnatte, Capucine aut Schmutzler, Rita K aut Wappenschmidt, Barbara aut Engel, Christoph aut Schönbuchner, Ines aut Deissler, Helmut aut Meindl, Alfons aut Hogervorst, Frans B aut Verheus, Martijn aut Hooning, Maartje J aut van den Ouweland, Ans MW aut Nelen, Marcel R aut Ausems, Margreet GEM aut Aalfs, Cora M aut van Asperen, Christi J aut Devilee, Peter aut Gerrits, Monique M aut Waisfisz, Quinten aut Szabo, Csilla I aut Easton, Douglas F aut Peock, Susan aut Cook, Margaret aut Oliver, Clare T aut Frost, Debra aut Harrington, Patricia aut Evans, D Gareth aut Lalloo, Fiona aut Eeles, Ros aut Izatt, Louise aut Chu, Carol aut Davidson, Rosemarie aut Eccles, Diana aut Ong, Kai-Ren aut Cook, Jackie aut Rebbeck, Tim aut Nathanson, Katherine L aut Domchek, Susan M aut Singer, Christian F aut Gschwantler-Kaulich, Daphne aut Dressler, Anne-Catharina aut Pfeiler, Georg aut Godwin, Andrew K aut Heikkinen, Tuomas aut Nevanlinna, Heli aut Agnarsson, Bjarni A aut Caligo, Maria Adelaide aut Olsson, Håkan aut Kristoffersson, Ulf aut Liljegren, Annelie aut Arver, Brita aut Karlsson, Per aut Melin, Beatrice aut Sinilnikova, Olga M aut McGuffog, Lesley aut Antoniou, Antonis C aut Chenevix-Trench, Georgia aut Spurdle, Amanda B aut Couch, Fergus J aut Enthalten in Breast cancer research London : BioMed Central, 1999 12(2010), 6 vom: 29. Nov. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:12 year:2010 number:6 day:29 month:11 https://dx.doi.org/10.1186/bcr2785 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2010 6 29 11 |
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Walker, Logan C @@aut@@ Fredericksen, Zachary S @@aut@@ Wang, Xianshu @@aut@@ Tarrell, Robert @@aut@@ Pankratz, Vernon S @@aut@@ Lindor, Noralane M @@aut@@ Beesley, Jonathan @@aut@@ Healey, Sue @@aut@@ Chen, Xiaoqing @@aut@@ Stoppa-Lyonnet, Dominique @@aut@@ Tirapo, Carole @@aut@@ Giraud, Sophie @@aut@@ Mazoyer, Sylvie @@aut@@ Muller, Danièle @@aut@@ Fricker, Jean-Pierre @@aut@@ Delnatte, Capucine @@aut@@ Schmutzler, Rita K @@aut@@ Wappenschmidt, Barbara @@aut@@ Engel, Christoph @@aut@@ Schönbuchner, Ines @@aut@@ Deissler, Helmut @@aut@@ Meindl, Alfons @@aut@@ Hogervorst, Frans B @@aut@@ Verheus, Martijn @@aut@@ Hooning, Maartje J @@aut@@ van den Ouweland, Ans MW @@aut@@ Nelen, Marcel R @@aut@@ Ausems, Margreet GEM @@aut@@ Aalfs, Cora M @@aut@@ van Asperen, Christi J @@aut@@ Devilee, Peter @@aut@@ Gerrits, Monique M @@aut@@ Waisfisz, Quinten @@aut@@ Szabo, Csilla I @@aut@@ Easton, Douglas F @@aut@@ Peock, Susan @@aut@@ Cook, Margaret @@aut@@ Oliver, Clare T @@aut@@ Frost, Debra @@aut@@ Harrington, Patricia @@aut@@ Evans, D Gareth @@aut@@ Lalloo, Fiona @@aut@@ Eeles, Ros @@aut@@ Izatt, Louise @@aut@@ Chu, Carol @@aut@@ Davidson, Rosemarie @@aut@@ Eccles, Diana @@aut@@ Ong, Kai-Ren @@aut@@ Cook, Jackie @@aut@@ Rebbeck, Tim @@aut@@ Nathanson, Katherine L @@aut@@ Domchek, Susan M @@aut@@ Singer, Christian F @@aut@@ Gschwantler-Kaulich, Daphne @@aut@@ Dressler, Anne-Catharina @@aut@@ Pfeiler, Georg @@aut@@ Godwin, Andrew K @@aut@@ Heikkinen, Tuomas @@aut@@ Nevanlinna, Heli @@aut@@ Agnarsson, Bjarni A @@aut@@ Caligo, Maria Adelaide @@aut@@ Olsson, Håkan @@aut@@ Kristoffersson, Ulf @@aut@@ Liljegren, Annelie @@aut@@ Arver, Brita @@aut@@ Karlsson, Per @@aut@@ Melin, Beatrice @@aut@@ Sinilnikova, Olga M @@aut@@ McGuffog, Lesley @@aut@@ Antoniou, Antonis C @@aut@@ Chenevix-Trench, Georgia @@aut@@ Spurdle, Amanda B @@aut@@ Couch, Fergus J @@aut@@ |
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This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate genes derived through a novel approach that analysed gene expression differences to prioritise candidate modifier genes for association studies. Methods We successfully genotyped 24 SNPs in a cohort of up to 4,724 BRCA1 and 2,693 BRCA2 female mutation carriers from 15 study groups and assessed whether these variants were associated with risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Results SNPs in five of the 14 candidate genes showed evidence of association with breast cancer risk for BRCA1 or BRCA2 carriers (P < 0.05). Notably, the minor alleles of two SNPs (rs7166081 and rs3825977) in high linkage disequilibrium (r2 = 0.77), located at the SMAD3 locus (15q22), were each associated with increased breast cancer risk for BRCA2 mutation carriers (relative risk = 1.25, 95% confidence interval = 1.07 to 1.45, Ptrend = 0.004; and relative risk = 1.20, 95% confidence interval = 1.03 to 1.40, Ptrend = 0.018). Conclusions This study provides evidence that the SMAD3 gene, which encodes a key regulatory protein in the transforming growth factor beta signalling pathway and is known to interact directly with BRCA2, may contribute to increased risk of breast cancer in BRCA2 mutation carriers. 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Walker, Logan C Fredericksen, Zachary S Wang, Xianshu Tarrell, Robert Pankratz, Vernon S Lindor, Noralane M Beesley, Jonathan Healey, Sue Chen, Xiaoqing Stoppa-Lyonnet, Dominique Tirapo, Carole Giraud, Sophie Mazoyer, Sylvie Muller, Danièle Fricker, Jean-Pierre Delnatte, Capucine Schmutzler, Rita K Wappenschmidt, Barbara Engel, Christoph Schönbuchner, Ines Deissler, Helmut Meindl, Alfons Hogervorst, Frans B Verheus, Martijn Hooning, Maartje J van den Ouweland, Ans MW Nelen, Marcel R Ausems, Margreet GEM Aalfs, Cora M van Asperen, Christi J Devilee, Peter Gerrits, Monique M Waisfisz, Quinten Szabo, Csilla I Easton, Douglas F Peock, Susan Cook, Margaret Oliver, Clare T Frost, Debra Harrington, Patricia Evans, D Gareth Lalloo, Fiona Eeles, Ros Izatt, Louise Chu, Carol Davidson, Rosemarie Eccles, Diana Ong, Kai-Ren Cook, Jackie Rebbeck, Tim Nathanson, Katherine L Domchek, Susan M Singer, Christian F Gschwantler-Kaulich, Daphne Dressler, Anne-Catharina Pfeiler, Georg Godwin, Andrew K Heikkinen, Tuomas Nevanlinna, Heli Agnarsson, Bjarni A Caligo, Maria Adelaide Olsson, Håkan Kristoffersson, Ulf Liljegren, Annelie Arver, Brita Karlsson, Per Melin, Beatrice Sinilnikova, Olga M McGuffog, Lesley Antoniou, Antonis C Chenevix-Trench, Georgia Spurdle, Amanda B Couch, Fergus J |
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evidence for smad3 as a modifier of breast cancer risk in brca2mutation carriers |
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Evidence for SMAD3 as a modifier of breast cancer risk in BRCA2mutation carriers |
| abstract |
Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate genes derived through a novel approach that analysed gene expression differences to prioritise candidate modifier genes for association studies. Methods We successfully genotyped 24 SNPs in a cohort of up to 4,724 BRCA1 and 2,693 BRCA2 female mutation carriers from 15 study groups and assessed whether these variants were associated with risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Results SNPs in five of the 14 candidate genes showed evidence of association with breast cancer risk for BRCA1 or BRCA2 carriers (P < 0.05). Notably, the minor alleles of two SNPs (rs7166081 and rs3825977) in high linkage disequilibrium (r2 = 0.77), located at the SMAD3 locus (15q22), were each associated with increased breast cancer risk for BRCA2 mutation carriers (relative risk = 1.25, 95% confidence interval = 1.07 to 1.45, Ptrend = 0.004; and relative risk = 1.20, 95% confidence interval = 1.03 to 1.40, Ptrend = 0.018). Conclusions This study provides evidence that the SMAD3 gene, which encodes a key regulatory protein in the transforming growth factor beta signalling pathway and is known to interact directly with BRCA2, may contribute to increased risk of breast cancer in BRCA2 mutation carriers. This finding suggests that genes with expression associated with BRCA1 and BRCA2 mutation status are enriched for the presence of common genetic modifiers of breast cancer risk in these populations. © Walker et al.; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| abstractGer |
Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate genes derived through a novel approach that analysed gene expression differences to prioritise candidate modifier genes for association studies. Methods We successfully genotyped 24 SNPs in a cohort of up to 4,724 BRCA1 and 2,693 BRCA2 female mutation carriers from 15 study groups and assessed whether these variants were associated with risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Results SNPs in five of the 14 candidate genes showed evidence of association with breast cancer risk for BRCA1 or BRCA2 carriers (P < 0.05). Notably, the minor alleles of two SNPs (rs7166081 and rs3825977) in high linkage disequilibrium (r2 = 0.77), located at the SMAD3 locus (15q22), were each associated with increased breast cancer risk for BRCA2 mutation carriers (relative risk = 1.25, 95% confidence interval = 1.07 to 1.45, Ptrend = 0.004; and relative risk = 1.20, 95% confidence interval = 1.03 to 1.40, Ptrend = 0.018). Conclusions This study provides evidence that the SMAD3 gene, which encodes a key regulatory protein in the transforming growth factor beta signalling pathway and is known to interact directly with BRCA2, may contribute to increased risk of breast cancer in BRCA2 mutation carriers. This finding suggests that genes with expression associated with BRCA1 and BRCA2 mutation status are enriched for the presence of common genetic modifiers of breast cancer risk in these populations. © Walker et al.; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| abstract_unstemmed |
Introduction Current attempts to identify genetic modifiers of BRCA1 and BRCA2 associated risk have focused on a candidate gene approach, based on knowledge of gene functions, or the development of large genome-wide association studies. In this study, we evaluated 24 SNPs tagged to 14 candidate genes derived through a novel approach that analysed gene expression differences to prioritise candidate modifier genes for association studies. Methods We successfully genotyped 24 SNPs in a cohort of up to 4,724 BRCA1 and 2,693 BRCA2 female mutation carriers from 15 study groups and assessed whether these variants were associated with risk of breast cancer in BRCA1 and BRCA2 mutation carriers. Results SNPs in five of the 14 candidate genes showed evidence of association with breast cancer risk for BRCA1 or BRCA2 carriers (P < 0.05). Notably, the minor alleles of two SNPs (rs7166081 and rs3825977) in high linkage disequilibrium (r2 = 0.77), located at the SMAD3 locus (15q22), were each associated with increased breast cancer risk for BRCA2 mutation carriers (relative risk = 1.25, 95% confidence interval = 1.07 to 1.45, Ptrend = 0.004; and relative risk = 1.20, 95% confidence interval = 1.03 to 1.40, Ptrend = 0.018). Conclusions This study provides evidence that the SMAD3 gene, which encodes a key regulatory protein in the transforming growth factor beta signalling pathway and is known to interact directly with BRCA2, may contribute to increased risk of breast cancer in BRCA2 mutation carriers. This finding suggests that genes with expression associated with BRCA1 and BRCA2 mutation status are enriched for the presence of common genetic modifiers of breast cancer risk in these populations. © Walker et al.; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
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Fredericksen, Zachary S Wang, Xianshu Tarrell, Robert Pankratz, Vernon S Lindor, Noralane M Beesley, Jonathan Healey, Sue Chen, Xiaoqing Stoppa-Lyonnet, Dominique Tirapo, Carole Giraud, Sophie Mazoyer, Sylvie Muller, Danièle Fricker, Jean-Pierre Delnatte, Capucine Schmutzler, Rita K Wappenschmidt, Barbara Engel, Christoph Schönbuchner, Ines Deissler, Helmut Meindl, Alfons Hogervorst, Frans B Verheus, Martijn Hooning, Maartje J van den Ouweland, Ans MW Nelen, Marcel R Ausems, Margreet GEM Aalfs, Cora M van Asperen, Christi J Devilee, Peter Gerrits, Monique M Waisfisz, Quinten Szabo, Csilla I Easton, Douglas F Peock, Susan Cook, Margaret Oliver, Clare T Frost, Debra Harrington, Patricia Evans, D Gareth Lalloo, Fiona Eeles, Ros Izatt, Louise Chu, Carol Davidson, Rosemarie Eccles, Diana Ong, Kai-Ren Cook, Jackie Rebbeck, Tim Nathanson, Katherine L Domchek, Susan M Singer, Christian F Gschwantler-Kaulich, Daphne Dressler, Anne-Catharina Pfeiler, Georg Godwin, Andrew K Heikkinen, Tuomas Nevanlinna, Heli Agnarsson, Bjarni A Caligo, Maria Adelaide Olsson, Håkan Kristoffersson, Ulf Liljegren, Annelie Arver, Brita Karlsson, Per Melin, Beatrice Sinilnikova, Olga M McGuffog, Lesley Antoniou, Antonis C Chenevix-Trench, Georgia Spurdle, Amanda B Couch, Fergus J |
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