An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers
Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitoch...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Blein, Sophie [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Schlagwörter: |
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| Anmerkung: |
© Blein et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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| Übergeordnetes Werk: |
Enthalten in: Breast cancer research - London : BioMed Central, 1999, 17(2015), 1 vom: 25. Apr. |
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| Übergeordnetes Werk: |
volume:17 ; year:2015 ; number:1 ; day:25 ; month:04 |
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| DOI / URN: |
10.1186/s13058-015-0567-2 |
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| Katalog-ID: |
SPR029955068 |
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| 100 | 1 | |a Blein, Sophie |e verfasserin |4 aut | |
| 245 | 1 | 3 | |a An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers |
| 264 | 1 | |c 2015 | |
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| 500 | |a © Blein et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( | ||
| 520 | |a Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects. | ||
| 650 | 4 | |a Breast Cancer |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Breast Cancer Risk |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Mitochondrial Genome |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Mutation Carrier |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a BRCA2 Mutation |7 (dpeaa)DE-He213 | |
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10.1186/s13058-015-0567-2 doi (DE-627)SPR029955068 (SPR)s13058-015-0567-2-e DE-627 ger DE-627 rakwb eng Blein, Sophie verfasserin aut An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Blein et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Mitochondrial Genome (dpeaa)DE-He213 Mutation Carrier (dpeaa)DE-He213 BRCA2 Mutation (dpeaa)DE-He213 Bardel, Claire aut Danjean, Vincent aut McGuffog, Lesley aut Healey, Sue aut Barrowdale, Daniel aut Lee, Andrew aut Dennis, Joe aut Kuchenbaecker, Karoline B aut Soucy, Penny aut Terry, Mary Beth aut Chung, Wendy K aut Goldgar, David E aut Buys, Saundra S aut Janavicius, Ramunas aut Tihomirova, Laima aut Tung, Nadine aut Dorfling, Cecilia M aut van Rensburg, Elizabeth J aut Neuhausen, Susan L aut Ding, Yuan Chun aut Gerdes, Anne-Marie aut Ejlertsen, Bent aut Nielsen, Finn C aut Hansen, Thomas VO aut Osorio, Ana aut Benitez, Javier aut Conejero, Raquel Andrés aut Segota, Ena aut Weitzel, Jeffrey N aut Thelander, Margo aut Peterlongo, Paolo aut Radice, Paolo aut Pensotti, Valeria aut Dolcetti, Riccardo aut Bonanni, Bernardo aut Peissel, Bernard aut Zaffaroni, Daniela aut Scuvera, Giulietta aut Manoukian, Siranoush aut Varesco, Liliana aut Capone, Gabriele L aut Papi, Laura aut Ottini, Laura aut Yannoukakos, Drakoulis aut Konstantopoulou, Irene aut Garber, Judy aut Hamann, Ute aut Donaldson, Alan aut Brady, Angela aut Brewer, Carole aut Foo, Claire aut Evans, D Gareth aut Frost, Debra aut Eccles, Diana aut Douglas, Fiona aut Cook, Jackie aut Adlard, Julian aut Barwell, Julian aut Walker, Lisa aut Izatt, Louise aut Side, Lucy E aut Kennedy, M John aut Tischkowitz, Marc aut Rogers, Mark T aut Porteous, Mary E aut Morrison, Patrick J aut Platte, Radka aut Eeles, Ros aut Davidson, Rosemarie aut Hodgson, Shirley aut Cole, Trevor aut Godwin, Andrew K aut Isaacs, Claudine aut Claes, Kathleen aut De Leeneer, Kim aut Meindl, Alfons aut Gehrig, Andrea aut Wappenschmidt, Barbara aut Sutter, Christian aut Engel, Christoph aut Niederacher, Dieter aut Steinemann, Doris aut Plendl, Hansjoerg aut Kast, Karin aut Rhiem, Kerstin aut Ditsch, Nina aut Arnold, Norbert aut Varon-Mateeva, Raymonda aut Schmutzler, Rita K aut Preisler-Adams, Sabine aut Markov, Nadja Bogdanova aut Wang-Gohrke, Shan aut de Pauw, Antoine aut Lefol, Cédrick aut Lasset, Christine aut Leroux, Dominique aut Rouleau, Etienne aut Damiola, Francesca aut Dreyfus, Hélène aut Barjhoux, Laure aut Golmard, Lisa aut Uhrhammer, Nancy aut Bonadona, Valérie aut Sornin, Valérie aut Bignon, Yves-Jean aut Carter, Jonathan aut Van Le, Linda aut Piedmonte, Marion aut DiSilvestro, Paul A aut de la Hoya, Miguel aut Caldes, Trinidad aut Nevanlinna, Heli aut Aittomäki, Kristiina aut Jager, Agnes aut van den Ouweland, Ans MW aut Kets, Carolien M aut Aalfs, Cora M aut van Leeuwen, Flora E aut Hogervorst, Frans BL aut Meijers-Heijboer, Hanne EJ aut Oosterwijk, Jan C aut van Roozendaal, Kees EP aut Rookus, Matti A aut Devilee, Peter aut van der Luijt, Rob B aut Olah, Edith aut Diez, Orland aut Teulé, Alex aut Lazaro, Conxi aut Blanco, Ignacio aut Del Valle, Jesús aut Jakubowska, Anna aut Sukiennicki, Grzegorz aut Gronwald, Jacek aut Lubinski, Jan aut Durda, Katarzyna aut Jaworska-Bieniek, Katarzyna aut Agnarsson, Bjarni A aut Maugard, Christine aut Amadori, Alberto aut Montagna, Marco aut Teixeira, Manuel R aut Spurdle, Amanda B aut Foulkes, William aut Olswold, Curtis aut Lindor, Noralane M aut Pankratz, Vernon S aut Szabo, Csilla I aut Lincoln, Anne aut Jacobs, Lauren aut Corines, Marina aut Robson, Mark aut Vijai, Joseph aut Berger, Andreas aut Fink-Retter, Anneliese aut Singer, Christian F aut Rappaport, Christine aut Kaulich, Daphne Geschwantler aut Pfeiler, Georg aut Tea, Muy-Kheng aut Greene, Mark H aut Mai, Phuong L aut Rennert, Gad aut Imyanitov, Evgeny N aut Mulligan, Anna Marie aut Glendon, Gord aut Andrulis, Irene L aut Tchatchou, Sandrine aut Toland, Amanda Ewart aut Pedersen, Inge Sokilde aut Thomassen, Mads aut Kruse, Torben A aut Jensen, Uffe Birk aut Caligo, Maria A aut Friedman, Eitan aut Zidan, Jamal aut Laitman, Yael aut Lindblom, Annika aut Melin, Beatrice aut Arver, Brita aut Loman, Niklas aut Rosenquist, Richard aut Olopade, Olufunmilayo I aut Nussbaum, Robert L aut Ramus, Susan J aut Nathanson, Katherine L aut Domchek, Susan M aut Rebbeck, Timothy R aut Arun, Banu K aut Mitchell, Gillian aut Karlan, Beth Y aut Lester, Jenny aut Orsulic, Sandra aut Stoppa-Lyonnet, Dominique aut Thomas, Gilles aut Simard, Jacques aut Couch, Fergus J aut Offit, Kenneth aut Easton, Douglas F aut Chenevix-Trench, Georgia aut Antoniou, Antonis C aut Mazoyer, Sylvie aut Phelan, Catherine M aut Sinilnikova, Olga M aut Cox, David G aut Enthalten in Breast cancer research London : BioMed Central, 1999 17(2015), 1 vom: 25. Apr. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:17 year:2015 number:1 day:25 month:04 https://dx.doi.org/10.1186/s13058-015-0567-2 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_2005 GBV_ILN_2014 GBV_ILN_2106 GBV_ILN_2232 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 17 2015 1 25 04 |
| spelling |
10.1186/s13058-015-0567-2 doi (DE-627)SPR029955068 (SPR)s13058-015-0567-2-e DE-627 ger DE-627 rakwb eng Blein, Sophie verfasserin aut An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Blein et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Mitochondrial Genome (dpeaa)DE-He213 Mutation Carrier (dpeaa)DE-He213 BRCA2 Mutation (dpeaa)DE-He213 Bardel, Claire aut Danjean, Vincent aut McGuffog, Lesley aut Healey, Sue aut Barrowdale, Daniel aut Lee, Andrew aut Dennis, Joe aut Kuchenbaecker, Karoline B aut Soucy, Penny aut Terry, Mary Beth aut Chung, Wendy K aut Goldgar, David E aut Buys, Saundra S aut Janavicius, Ramunas aut Tihomirova, Laima aut Tung, Nadine aut Dorfling, Cecilia M aut van Rensburg, Elizabeth J aut Neuhausen, Susan L aut Ding, Yuan Chun aut Gerdes, Anne-Marie aut Ejlertsen, Bent aut Nielsen, Finn C aut Hansen, Thomas VO aut Osorio, Ana aut Benitez, Javier aut Conejero, Raquel Andrés aut Segota, Ena aut Weitzel, Jeffrey N aut Thelander, Margo aut Peterlongo, Paolo aut Radice, Paolo aut Pensotti, Valeria aut Dolcetti, Riccardo aut Bonanni, Bernardo aut Peissel, Bernard aut Zaffaroni, Daniela aut Scuvera, Giulietta aut Manoukian, Siranoush aut Varesco, Liliana aut Capone, Gabriele L aut Papi, Laura aut Ottini, Laura aut Yannoukakos, Drakoulis aut Konstantopoulou, Irene aut Garber, Judy aut Hamann, Ute aut Donaldson, Alan aut Brady, Angela aut Brewer, Carole aut Foo, Claire aut Evans, D Gareth aut Frost, Debra aut Eccles, Diana aut Douglas, Fiona aut Cook, Jackie aut Adlard, Julian aut Barwell, Julian aut Walker, Lisa aut Izatt, Louise aut Side, Lucy E aut Kennedy, M John aut Tischkowitz, Marc aut Rogers, Mark T aut Porteous, Mary E aut Morrison, Patrick J aut Platte, Radka aut Eeles, Ros aut Davidson, Rosemarie aut Hodgson, Shirley aut Cole, Trevor aut Godwin, Andrew K aut Isaacs, Claudine aut Claes, Kathleen aut De Leeneer, Kim aut Meindl, Alfons aut Gehrig, Andrea aut Wappenschmidt, Barbara aut Sutter, Christian aut Engel, Christoph aut Niederacher, Dieter aut Steinemann, Doris aut Plendl, Hansjoerg aut Kast, Karin aut Rhiem, Kerstin aut Ditsch, Nina aut Arnold, Norbert aut Varon-Mateeva, Raymonda aut Schmutzler, Rita K aut Preisler-Adams, Sabine aut Markov, Nadja Bogdanova aut Wang-Gohrke, Shan aut de Pauw, Antoine aut Lefol, Cédrick aut Lasset, Christine aut Leroux, Dominique aut Rouleau, Etienne aut Damiola, Francesca aut Dreyfus, Hélène aut Barjhoux, Laure aut Golmard, Lisa aut Uhrhammer, Nancy aut Bonadona, Valérie aut Sornin, Valérie aut Bignon, Yves-Jean aut Carter, Jonathan aut Van Le, Linda aut Piedmonte, Marion aut DiSilvestro, Paul A aut de la Hoya, Miguel aut Caldes, Trinidad aut Nevanlinna, Heli aut Aittomäki, Kristiina aut Jager, Agnes aut van den Ouweland, Ans MW aut Kets, Carolien M aut Aalfs, Cora M aut van Leeuwen, Flora E aut Hogervorst, Frans BL aut Meijers-Heijboer, Hanne EJ aut Oosterwijk, Jan C aut van Roozendaal, Kees EP aut Rookus, Matti A aut Devilee, Peter aut van der Luijt, Rob B aut Olah, Edith aut Diez, Orland aut Teulé, Alex aut Lazaro, Conxi aut Blanco, Ignacio aut Del Valle, Jesús aut Jakubowska, Anna aut Sukiennicki, Grzegorz aut Gronwald, Jacek aut Lubinski, Jan aut Durda, Katarzyna aut Jaworska-Bieniek, Katarzyna aut Agnarsson, Bjarni A aut Maugard, Christine aut Amadori, Alberto aut Montagna, Marco aut Teixeira, Manuel R aut Spurdle, Amanda B aut Foulkes, William aut Olswold, Curtis aut Lindor, Noralane M aut Pankratz, Vernon S aut Szabo, Csilla I aut Lincoln, Anne aut Jacobs, Lauren aut Corines, Marina aut Robson, Mark aut Vijai, Joseph aut Berger, Andreas aut Fink-Retter, Anneliese aut Singer, Christian F aut Rappaport, Christine aut Kaulich, Daphne Geschwantler aut Pfeiler, Georg aut Tea, Muy-Kheng aut Greene, Mark H aut Mai, Phuong L aut Rennert, Gad aut Imyanitov, Evgeny N aut Mulligan, Anna Marie aut Glendon, Gord aut Andrulis, Irene L aut Tchatchou, Sandrine aut Toland, Amanda Ewart aut Pedersen, Inge Sokilde aut Thomassen, Mads aut Kruse, Torben A aut Jensen, Uffe Birk aut Caligo, Maria A aut Friedman, Eitan aut Zidan, Jamal aut Laitman, Yael aut Lindblom, Annika aut Melin, Beatrice aut Arver, Brita aut Loman, Niklas aut Rosenquist, Richard aut Olopade, Olufunmilayo I aut Nussbaum, Robert L aut Ramus, Susan J aut Nathanson, Katherine L aut Domchek, Susan M aut Rebbeck, Timothy R aut Arun, Banu K aut Mitchell, Gillian aut Karlan, Beth Y aut Lester, Jenny aut Orsulic, Sandra aut Stoppa-Lyonnet, Dominique aut Thomas, Gilles aut Simard, Jacques aut Couch, Fergus J aut Offit, Kenneth aut Easton, Douglas F aut Chenevix-Trench, Georgia aut Antoniou, Antonis C aut Mazoyer, Sylvie aut Phelan, Catherine M aut Sinilnikova, Olga M aut Cox, David G aut Enthalten in Breast cancer research London : BioMed Central, 1999 17(2015), 1 vom: 25. Apr. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:17 year:2015 number:1 day:25 month:04 https://dx.doi.org/10.1186/s13058-015-0567-2 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_2005 GBV_ILN_2014 GBV_ILN_2106 GBV_ILN_2232 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 17 2015 1 25 04 |
| allfields_unstemmed |
10.1186/s13058-015-0567-2 doi (DE-627)SPR029955068 (SPR)s13058-015-0567-2-e DE-627 ger DE-627 rakwb eng Blein, Sophie verfasserin aut An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Blein et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Mitochondrial Genome (dpeaa)DE-He213 Mutation Carrier (dpeaa)DE-He213 BRCA2 Mutation (dpeaa)DE-He213 Bardel, Claire aut Danjean, Vincent aut McGuffog, Lesley aut Healey, Sue aut Barrowdale, Daniel aut Lee, Andrew aut Dennis, Joe aut Kuchenbaecker, Karoline B aut Soucy, Penny aut Terry, Mary Beth aut Chung, Wendy K aut Goldgar, David E aut Buys, Saundra S aut Janavicius, Ramunas aut Tihomirova, Laima aut Tung, Nadine aut Dorfling, Cecilia M aut van Rensburg, Elizabeth J aut Neuhausen, Susan L aut Ding, Yuan Chun aut Gerdes, Anne-Marie aut Ejlertsen, Bent aut Nielsen, Finn C aut Hansen, Thomas VO aut Osorio, Ana aut Benitez, Javier aut Conejero, Raquel Andrés aut Segota, Ena aut Weitzel, Jeffrey N aut Thelander, Margo aut Peterlongo, Paolo aut Radice, Paolo aut Pensotti, Valeria aut Dolcetti, Riccardo aut Bonanni, Bernardo aut Peissel, Bernard aut Zaffaroni, Daniela aut Scuvera, Giulietta aut Manoukian, Siranoush aut Varesco, Liliana aut Capone, Gabriele L aut Papi, Laura aut Ottini, Laura aut Yannoukakos, Drakoulis aut Konstantopoulou, Irene aut Garber, Judy aut Hamann, Ute aut Donaldson, Alan aut Brady, Angela aut Brewer, Carole aut Foo, Claire aut Evans, D Gareth aut Frost, Debra aut Eccles, Diana aut Douglas, Fiona aut Cook, Jackie aut Adlard, Julian aut Barwell, Julian aut Walker, Lisa aut Izatt, Louise aut Side, Lucy E aut Kennedy, M John aut Tischkowitz, Marc aut Rogers, Mark T aut Porteous, Mary E aut Morrison, Patrick J aut Platte, Radka aut Eeles, Ros aut Davidson, Rosemarie aut Hodgson, Shirley aut Cole, Trevor aut Godwin, Andrew K aut Isaacs, Claudine aut Claes, Kathleen aut De Leeneer, Kim aut Meindl, Alfons aut Gehrig, Andrea aut Wappenschmidt, Barbara aut Sutter, Christian aut Engel, Christoph aut Niederacher, Dieter aut Steinemann, Doris aut Plendl, Hansjoerg aut Kast, Karin aut Rhiem, Kerstin aut Ditsch, Nina aut Arnold, Norbert aut Varon-Mateeva, Raymonda aut Schmutzler, Rita K aut Preisler-Adams, Sabine aut Markov, Nadja Bogdanova aut Wang-Gohrke, Shan aut de Pauw, Antoine aut Lefol, Cédrick aut Lasset, Christine aut Leroux, Dominique aut Rouleau, Etienne aut Damiola, Francesca aut Dreyfus, Hélène aut Barjhoux, Laure aut Golmard, Lisa aut Uhrhammer, Nancy aut Bonadona, Valérie aut Sornin, Valérie aut Bignon, Yves-Jean aut Carter, Jonathan aut Van Le, Linda aut Piedmonte, Marion aut DiSilvestro, Paul A aut de la Hoya, Miguel aut Caldes, Trinidad aut Nevanlinna, Heli aut Aittomäki, Kristiina aut Jager, Agnes aut van den Ouweland, Ans MW aut Kets, Carolien M aut Aalfs, Cora M aut van Leeuwen, Flora E aut Hogervorst, Frans BL aut Meijers-Heijboer, Hanne EJ aut Oosterwijk, Jan C aut van Roozendaal, Kees EP aut Rookus, Matti A aut Devilee, Peter aut van der Luijt, Rob B aut Olah, Edith aut Diez, Orland aut Teulé, Alex aut Lazaro, Conxi aut Blanco, Ignacio aut Del Valle, Jesús aut Jakubowska, Anna aut Sukiennicki, Grzegorz aut Gronwald, Jacek aut Lubinski, Jan aut Durda, Katarzyna aut Jaworska-Bieniek, Katarzyna aut Agnarsson, Bjarni A aut Maugard, Christine aut Amadori, Alberto aut Montagna, Marco aut Teixeira, Manuel R aut Spurdle, Amanda B aut Foulkes, William aut Olswold, Curtis aut Lindor, Noralane M aut Pankratz, Vernon S aut Szabo, Csilla I aut Lincoln, Anne aut Jacobs, Lauren aut Corines, Marina aut Robson, Mark aut Vijai, Joseph aut Berger, Andreas aut Fink-Retter, Anneliese aut Singer, Christian F aut Rappaport, Christine aut Kaulich, Daphne Geschwantler aut Pfeiler, Georg aut Tea, Muy-Kheng aut Greene, Mark H aut Mai, Phuong L aut Rennert, Gad aut Imyanitov, Evgeny N aut Mulligan, Anna Marie aut Glendon, Gord aut Andrulis, Irene L aut Tchatchou, Sandrine aut Toland, Amanda Ewart aut Pedersen, Inge Sokilde aut Thomassen, Mads aut Kruse, Torben A aut Jensen, Uffe Birk aut Caligo, Maria A aut Friedman, Eitan aut Zidan, Jamal aut Laitman, Yael aut Lindblom, Annika aut Melin, Beatrice aut Arver, Brita aut Loman, Niklas aut Rosenquist, Richard aut Olopade, Olufunmilayo I aut Nussbaum, Robert L aut Ramus, Susan J aut Nathanson, Katherine L aut Domchek, Susan M aut Rebbeck, Timothy R aut Arun, Banu K aut Mitchell, Gillian aut Karlan, Beth Y aut Lester, Jenny aut Orsulic, Sandra aut Stoppa-Lyonnet, Dominique aut Thomas, Gilles aut Simard, Jacques aut Couch, Fergus J aut Offit, Kenneth aut Easton, Douglas F aut Chenevix-Trench, Georgia aut Antoniou, Antonis C aut Mazoyer, Sylvie aut Phelan, Catherine M aut Sinilnikova, Olga M aut Cox, David G aut Enthalten in Breast cancer research London : BioMed Central, 1999 17(2015), 1 vom: 25. Apr. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:17 year:2015 number:1 day:25 month:04 https://dx.doi.org/10.1186/s13058-015-0567-2 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_2005 GBV_ILN_2014 GBV_ILN_2106 GBV_ILN_2232 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 17 2015 1 25 04 |
| allfieldsGer |
10.1186/s13058-015-0567-2 doi (DE-627)SPR029955068 (SPR)s13058-015-0567-2-e DE-627 ger DE-627 rakwb eng Blein, Sophie verfasserin aut An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Blein et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Mitochondrial Genome (dpeaa)DE-He213 Mutation Carrier (dpeaa)DE-He213 BRCA2 Mutation (dpeaa)DE-He213 Bardel, Claire aut Danjean, Vincent aut McGuffog, Lesley aut Healey, Sue aut Barrowdale, Daniel aut Lee, Andrew aut Dennis, Joe aut Kuchenbaecker, Karoline B aut Soucy, Penny aut Terry, Mary Beth aut Chung, Wendy K aut Goldgar, David E aut Buys, Saundra S aut Janavicius, Ramunas aut Tihomirova, Laima aut Tung, Nadine aut Dorfling, Cecilia M aut van Rensburg, Elizabeth J aut Neuhausen, Susan L aut Ding, Yuan Chun aut Gerdes, Anne-Marie aut Ejlertsen, Bent aut Nielsen, Finn C aut Hansen, Thomas VO aut Osorio, Ana aut Benitez, Javier aut Conejero, Raquel Andrés aut Segota, Ena aut Weitzel, Jeffrey N aut Thelander, Margo aut Peterlongo, Paolo aut Radice, Paolo aut Pensotti, Valeria aut Dolcetti, Riccardo aut Bonanni, Bernardo aut Peissel, Bernard aut Zaffaroni, Daniela aut Scuvera, Giulietta aut Manoukian, Siranoush aut Varesco, Liliana aut Capone, Gabriele L aut Papi, Laura aut Ottini, Laura aut Yannoukakos, Drakoulis aut Konstantopoulou, Irene aut Garber, Judy aut Hamann, Ute aut Donaldson, Alan aut Brady, Angela aut Brewer, Carole aut Foo, Claire aut Evans, D Gareth aut Frost, Debra aut Eccles, Diana aut Douglas, Fiona aut Cook, Jackie aut Adlard, Julian aut Barwell, Julian aut Walker, Lisa aut Izatt, Louise aut Side, Lucy E aut Kennedy, M John aut Tischkowitz, Marc aut Rogers, Mark T aut Porteous, Mary E aut Morrison, Patrick J aut Platte, Radka aut Eeles, Ros aut Davidson, Rosemarie aut Hodgson, Shirley aut Cole, Trevor aut Godwin, Andrew K aut Isaacs, Claudine aut Claes, Kathleen aut De Leeneer, Kim aut Meindl, Alfons aut Gehrig, Andrea aut Wappenschmidt, Barbara aut Sutter, Christian aut Engel, Christoph aut Niederacher, Dieter aut Steinemann, Doris aut Plendl, Hansjoerg aut Kast, Karin aut Rhiem, Kerstin aut Ditsch, Nina aut Arnold, Norbert aut Varon-Mateeva, Raymonda aut Schmutzler, Rita K aut Preisler-Adams, Sabine aut Markov, Nadja Bogdanova aut Wang-Gohrke, Shan aut de Pauw, Antoine aut Lefol, Cédrick aut Lasset, Christine aut Leroux, Dominique aut Rouleau, Etienne aut Damiola, Francesca aut Dreyfus, Hélène aut Barjhoux, Laure aut Golmard, Lisa aut Uhrhammer, Nancy aut Bonadona, Valérie aut Sornin, Valérie aut Bignon, Yves-Jean aut Carter, Jonathan aut Van Le, Linda aut Piedmonte, Marion aut DiSilvestro, Paul A aut de la Hoya, Miguel aut Caldes, Trinidad aut Nevanlinna, Heli aut Aittomäki, Kristiina aut Jager, Agnes aut van den Ouweland, Ans MW aut Kets, Carolien M aut Aalfs, Cora M aut van Leeuwen, Flora E aut Hogervorst, Frans BL aut Meijers-Heijboer, Hanne EJ aut Oosterwijk, Jan C aut van Roozendaal, Kees EP aut Rookus, Matti A aut Devilee, Peter aut van der Luijt, Rob B aut Olah, Edith aut Diez, Orland aut Teulé, Alex aut Lazaro, Conxi aut Blanco, Ignacio aut Del Valle, Jesús aut Jakubowska, Anna aut Sukiennicki, Grzegorz aut Gronwald, Jacek aut Lubinski, Jan aut Durda, Katarzyna aut Jaworska-Bieniek, Katarzyna aut Agnarsson, Bjarni A aut Maugard, Christine aut Amadori, Alberto aut Montagna, Marco aut Teixeira, Manuel R aut Spurdle, Amanda B aut Foulkes, William aut Olswold, Curtis aut Lindor, Noralane M aut Pankratz, Vernon S aut Szabo, Csilla I aut Lincoln, Anne aut Jacobs, Lauren aut Corines, Marina aut Robson, Mark aut Vijai, Joseph aut Berger, Andreas aut Fink-Retter, Anneliese aut Singer, Christian F aut Rappaport, Christine aut Kaulich, Daphne Geschwantler aut Pfeiler, Georg aut Tea, Muy-Kheng aut Greene, Mark H aut Mai, Phuong L aut Rennert, Gad aut Imyanitov, Evgeny N aut Mulligan, Anna Marie aut Glendon, Gord aut Andrulis, Irene L aut Tchatchou, Sandrine aut Toland, Amanda Ewart aut Pedersen, Inge Sokilde aut Thomassen, Mads aut Kruse, Torben A aut Jensen, Uffe Birk aut Caligo, Maria A aut Friedman, Eitan aut Zidan, Jamal aut Laitman, Yael aut Lindblom, Annika aut Melin, Beatrice aut Arver, Brita aut Loman, Niklas aut Rosenquist, Richard aut Olopade, Olufunmilayo I aut Nussbaum, Robert L aut Ramus, Susan J aut Nathanson, Katherine L aut Domchek, Susan M aut Rebbeck, Timothy R aut Arun, Banu K aut Mitchell, Gillian aut Karlan, Beth Y aut Lester, Jenny aut Orsulic, Sandra aut Stoppa-Lyonnet, Dominique aut Thomas, Gilles aut Simard, Jacques aut Couch, Fergus J aut Offit, Kenneth aut Easton, Douglas F aut Chenevix-Trench, Georgia aut Antoniou, Antonis C aut Mazoyer, Sylvie aut Phelan, Catherine M aut Sinilnikova, Olga M aut Cox, David G aut Enthalten in Breast cancer research London : BioMed Central, 1999 17(2015), 1 vom: 25. Apr. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:17 year:2015 number:1 day:25 month:04 https://dx.doi.org/10.1186/s13058-015-0567-2 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_2005 GBV_ILN_2014 GBV_ILN_2106 GBV_ILN_2232 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 17 2015 1 25 04 |
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10.1186/s13058-015-0567-2 doi (DE-627)SPR029955068 (SPR)s13058-015-0567-2-e DE-627 ger DE-627 rakwb eng Blein, Sophie verfasserin aut An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Blein et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects. Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Mitochondrial Genome (dpeaa)DE-He213 Mutation Carrier (dpeaa)DE-He213 BRCA2 Mutation (dpeaa)DE-He213 Bardel, Claire aut Danjean, Vincent aut McGuffog, Lesley aut Healey, Sue aut Barrowdale, Daniel aut Lee, Andrew aut Dennis, Joe aut Kuchenbaecker, Karoline B aut Soucy, Penny aut Terry, Mary Beth aut Chung, Wendy K aut Goldgar, David E aut Buys, Saundra S aut Janavicius, Ramunas aut Tihomirova, Laima aut Tung, Nadine aut Dorfling, Cecilia M aut van Rensburg, Elizabeth J aut Neuhausen, Susan L aut Ding, Yuan Chun aut Gerdes, Anne-Marie aut Ejlertsen, Bent aut Nielsen, Finn C aut Hansen, Thomas VO aut Osorio, Ana aut Benitez, Javier aut Conejero, Raquel Andrés aut Segota, Ena aut Weitzel, Jeffrey N aut Thelander, Margo aut Peterlongo, Paolo aut Radice, Paolo aut Pensotti, Valeria aut Dolcetti, Riccardo aut Bonanni, Bernardo aut Peissel, Bernard aut Zaffaroni, Daniela aut Scuvera, Giulietta aut Manoukian, Siranoush aut Varesco, Liliana aut Capone, Gabriele L aut Papi, Laura aut Ottini, Laura aut Yannoukakos, Drakoulis aut Konstantopoulou, Irene aut Garber, Judy aut Hamann, Ute aut Donaldson, Alan aut Brady, Angela aut Brewer, Carole aut Foo, Claire aut Evans, D Gareth aut Frost, Debra aut Eccles, Diana aut Douglas, Fiona aut Cook, Jackie aut Adlard, Julian aut Barwell, Julian aut Walker, Lisa aut Izatt, Louise aut Side, Lucy E aut Kennedy, M John aut Tischkowitz, Marc aut Rogers, Mark T aut Porteous, Mary E aut Morrison, Patrick J aut Platte, Radka aut Eeles, Ros aut Davidson, Rosemarie aut Hodgson, Shirley aut Cole, Trevor aut Godwin, Andrew K aut Isaacs, Claudine aut Claes, Kathleen aut De Leeneer, Kim aut Meindl, Alfons aut Gehrig, Andrea aut Wappenschmidt, Barbara aut Sutter, Christian aut Engel, Christoph aut Niederacher, Dieter aut Steinemann, Doris aut Plendl, Hansjoerg aut Kast, Karin aut Rhiem, Kerstin aut Ditsch, Nina aut Arnold, Norbert aut Varon-Mateeva, Raymonda aut Schmutzler, Rita K aut Preisler-Adams, Sabine aut Markov, Nadja Bogdanova aut Wang-Gohrke, Shan aut de Pauw, Antoine aut Lefol, Cédrick aut Lasset, Christine aut Leroux, Dominique aut Rouleau, Etienne aut Damiola, Francesca aut Dreyfus, Hélène aut Barjhoux, Laure aut Golmard, Lisa aut Uhrhammer, Nancy aut Bonadona, Valérie aut Sornin, Valérie aut Bignon, Yves-Jean aut Carter, Jonathan aut Van Le, Linda aut Piedmonte, Marion aut DiSilvestro, Paul A aut de la Hoya, Miguel aut Caldes, Trinidad aut Nevanlinna, Heli aut Aittomäki, Kristiina aut Jager, Agnes aut van den Ouweland, Ans MW aut Kets, Carolien M aut Aalfs, Cora M aut van Leeuwen, Flora E aut Hogervorst, Frans BL aut Meijers-Heijboer, Hanne EJ aut Oosterwijk, Jan C aut van Roozendaal, Kees EP aut Rookus, Matti A aut Devilee, Peter aut van der Luijt, Rob B aut Olah, Edith aut Diez, Orland aut Teulé, Alex aut Lazaro, Conxi aut Blanco, Ignacio aut Del Valle, Jesús aut Jakubowska, Anna aut Sukiennicki, Grzegorz aut Gronwald, Jacek aut Lubinski, Jan aut Durda, Katarzyna aut Jaworska-Bieniek, Katarzyna aut Agnarsson, Bjarni A aut Maugard, Christine aut Amadori, Alberto aut Montagna, Marco aut Teixeira, Manuel R aut Spurdle, Amanda B aut Foulkes, William aut Olswold, Curtis aut Lindor, Noralane M aut Pankratz, Vernon S aut Szabo, Csilla I aut Lincoln, Anne aut Jacobs, Lauren aut Corines, Marina aut Robson, Mark aut Vijai, Joseph aut Berger, Andreas aut Fink-Retter, Anneliese aut Singer, Christian F aut Rappaport, Christine aut Kaulich, Daphne Geschwantler aut Pfeiler, Georg aut Tea, Muy-Kheng aut Greene, Mark H aut Mai, Phuong L aut Rennert, Gad aut Imyanitov, Evgeny N aut Mulligan, Anna Marie aut Glendon, Gord aut Andrulis, Irene L aut Tchatchou, Sandrine aut Toland, Amanda Ewart aut Pedersen, Inge Sokilde aut Thomassen, Mads aut Kruse, Torben A aut Jensen, Uffe Birk aut Caligo, Maria A aut Friedman, Eitan aut Zidan, Jamal aut Laitman, Yael aut Lindblom, Annika aut Melin, Beatrice aut Arver, Brita aut Loman, Niklas aut Rosenquist, Richard aut Olopade, Olufunmilayo I aut Nussbaum, Robert L aut Ramus, Susan J aut Nathanson, Katherine L aut Domchek, Susan M aut Rebbeck, Timothy R aut Arun, Banu K aut Mitchell, Gillian aut Karlan, Beth Y aut Lester, Jenny aut Orsulic, Sandra aut Stoppa-Lyonnet, Dominique aut Thomas, Gilles aut Simard, Jacques aut Couch, Fergus J aut Offit, Kenneth aut Easton, Douglas F aut Chenevix-Trench, Georgia aut Antoniou, Antonis C aut Mazoyer, Sylvie aut Phelan, Catherine M aut Sinilnikova, Olga M aut Cox, David G aut Enthalten in Breast cancer research London : BioMed Central, 1999 17(2015), 1 vom: 25. Apr. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:17 year:2015 number:1 day:25 month:04 https://dx.doi.org/10.1186/s13058-015-0567-2 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_2005 GBV_ILN_2014 GBV_ILN_2106 GBV_ILN_2232 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 17 2015 1 25 04 |
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Blein, Sophie @@aut@@ Bardel, Claire @@aut@@ Danjean, Vincent @@aut@@ McGuffog, Lesley @@aut@@ Healey, Sue @@aut@@ Barrowdale, Daniel @@aut@@ Lee, Andrew @@aut@@ Dennis, Joe @@aut@@ Kuchenbaecker, Karoline B @@aut@@ Soucy, Penny @@aut@@ Terry, Mary Beth @@aut@@ Chung, Wendy K @@aut@@ Goldgar, David E @@aut@@ Buys, Saundra S @@aut@@ Janavicius, Ramunas @@aut@@ Tihomirova, Laima @@aut@@ Tung, Nadine @@aut@@ Dorfling, Cecilia M @@aut@@ van Rensburg, Elizabeth J @@aut@@ Neuhausen, Susan L @@aut@@ Ding, Yuan Chun @@aut@@ Gerdes, Anne-Marie @@aut@@ Ejlertsen, Bent @@aut@@ Nielsen, Finn C @@aut@@ Hansen, Thomas VO @@aut@@ Osorio, Ana @@aut@@ Benitez, Javier @@aut@@ Conejero, Raquel Andrés @@aut@@ Segota, Ena @@aut@@ Weitzel, Jeffrey N @@aut@@ Thelander, Margo @@aut@@ Peterlongo, Paolo @@aut@@ Radice, Paolo @@aut@@ Pensotti, Valeria @@aut@@ Dolcetti, Riccardo @@aut@@ Bonanni, Bernardo @@aut@@ Peissel, Bernard @@aut@@ Zaffaroni, Daniela @@aut@@ Scuvera, Giulietta @@aut@@ Manoukian, Siranoush @@aut@@ Varesco, Liliana @@aut@@ Capone, Gabriele L @@aut@@ Papi, Laura @@aut@@ Ottini, Laura @@aut@@ Yannoukakos, Drakoulis @@aut@@ Konstantopoulou, Irene @@aut@@ Garber, Judy @@aut@@ Hamann, Ute @@aut@@ Donaldson, Alan @@aut@@ Brady, Angela @@aut@@ Brewer, Carole @@aut@@ Foo, Claire @@aut@@ Evans, D Gareth @@aut@@ Frost, Debra @@aut@@ Eccles, Diana @@aut@@ Douglas, Fiona @@aut@@ Cook, Jackie @@aut@@ Adlard, Julian @@aut@@ Barwell, Julian @@aut@@ Walker, Lisa @@aut@@ Izatt, Louise @@aut@@ Side, Lucy E @@aut@@ Kennedy, M John @@aut@@ Tischkowitz, Marc @@aut@@ Rogers, Mark T @@aut@@ Porteous, Mary E @@aut@@ Morrison, Patrick J @@aut@@ Platte, Radka @@aut@@ Eeles, Ros @@aut@@ Davidson, Rosemarie @@aut@@ Hodgson, Shirley @@aut@@ Cole, Trevor @@aut@@ Godwin, Andrew K @@aut@@ Isaacs, Claudine @@aut@@ Claes, Kathleen @@aut@@ De Leeneer, Kim @@aut@@ Meindl, Alfons @@aut@@ Gehrig, Andrea @@aut@@ Wappenschmidt, Barbara @@aut@@ Sutter, Christian @@aut@@ Engel, Christoph @@aut@@ Niederacher, Dieter @@aut@@ Steinemann, Doris @@aut@@ Plendl, Hansjoerg @@aut@@ Kast, Karin @@aut@@ Rhiem, Kerstin @@aut@@ Ditsch, Nina @@aut@@ Arnold, Norbert @@aut@@ Varon-Mateeva, Raymonda @@aut@@ Schmutzler, Rita K @@aut@@ Preisler-Adams, Sabine @@aut@@ Markov, Nadja Bogdanova @@aut@@ Wang-Gohrke, Shan @@aut@@ de Pauw, Antoine @@aut@@ Lefol, Cédrick @@aut@@ Lasset, Christine @@aut@@ Leroux, Dominique @@aut@@ Rouleau, Etienne @@aut@@ Damiola, Francesca @@aut@@ Dreyfus, Hélène @@aut@@ Barjhoux, Laure @@aut@@ Golmard, Lisa @@aut@@ Uhrhammer, Nancy @@aut@@ Bonadona, Valérie @@aut@@ Sornin, Valérie @@aut@@ Bignon, Yves-Jean @@aut@@ Carter, Jonathan @@aut@@ Van Le, Linda @@aut@@ Piedmonte, Marion @@aut@@ DiSilvestro, Paul A @@aut@@ de la Hoya, Miguel @@aut@@ Caldes, Trinidad @@aut@@ Nevanlinna, Heli @@aut@@ Aittomäki, Kristiina @@aut@@ Jager, Agnes @@aut@@ van den Ouweland, Ans MW @@aut@@ Kets, Carolien M @@aut@@ Aalfs, Cora M @@aut@@ van Leeuwen, Flora E @@aut@@ Hogervorst, Frans BL @@aut@@ Meijers-Heijboer, Hanne EJ @@aut@@ Oosterwijk, Jan C @@aut@@ van Roozendaal, Kees EP @@aut@@ Rookus, Matti A @@aut@@ Devilee, Peter @@aut@@ van der Luijt, Rob B @@aut@@ Olah, Edith @@aut@@ Diez, Orland @@aut@@ Teulé, Alex @@aut@@ Lazaro, Conxi @@aut@@ Blanco, Ignacio @@aut@@ Del Valle, Jesús @@aut@@ Jakubowska, Anna @@aut@@ Sukiennicki, Grzegorz @@aut@@ Gronwald, Jacek @@aut@@ Lubinski, Jan @@aut@@ Durda, Katarzyna @@aut@@ Jaworska-Bieniek, Katarzyna @@aut@@ Agnarsson, Bjarni A @@aut@@ Maugard, Christine @@aut@@ Amadori, Alberto @@aut@@ Montagna, Marco @@aut@@ Teixeira, Manuel R @@aut@@ Spurdle, Amanda B @@aut@@ Foulkes, William @@aut@@ Olswold, Curtis @@aut@@ Lindor, Noralane M @@aut@@ Pankratz, Vernon S @@aut@@ Szabo, Csilla I @@aut@@ Lincoln, Anne @@aut@@ Jacobs, Lauren @@aut@@ Corines, Marina @@aut@@ Robson, Mark @@aut@@ Vijai, Joseph @@aut@@ Berger, Andreas @@aut@@ Fink-Retter, Anneliese @@aut@@ Singer, Christian F @@aut@@ Rappaport, Christine @@aut@@ Kaulich, Daphne Geschwantler @@aut@@ Pfeiler, Georg @@aut@@ Tea, Muy-Kheng @@aut@@ Greene, Mark H @@aut@@ Mai, Phuong L @@aut@@ Rennert, Gad @@aut@@ Imyanitov, Evgeny N @@aut@@ Mulligan, Anna Marie @@aut@@ Glendon, Gord @@aut@@ Andrulis, Irene L @@aut@@ Tchatchou, Sandrine @@aut@@ Toland, Amanda Ewart @@aut@@ Pedersen, Inge Sokilde @@aut@@ Thomassen, Mads @@aut@@ Kruse, Torben A @@aut@@ Jensen, Uffe Birk @@aut@@ Caligo, Maria A @@aut@@ Friedman, Eitan @@aut@@ Zidan, Jamal @@aut@@ Laitman, Yael @@aut@@ Lindblom, Annika @@aut@@ Melin, Beatrice @@aut@@ Arver, Brita @@aut@@ Loman, Niklas @@aut@@ Rosenquist, Richard @@aut@@ Olopade, Olufunmilayo I @@aut@@ Nussbaum, Robert L @@aut@@ Ramus, Susan J @@aut@@ Nathanson, Katherine L @@aut@@ Domchek, Susan M @@aut@@ Rebbeck, Timothy R @@aut@@ Arun, Banu K @@aut@@ Mitchell, Gillian @@aut@@ Karlan, Beth Y @@aut@@ Lester, Jenny @@aut@@ Orsulic, Sandra @@aut@@ Stoppa-Lyonnet, Dominique @@aut@@ Thomas, Gilles @@aut@@ Simard, Jacques @@aut@@ Couch, Fergus J @@aut@@ Offit, Kenneth @@aut@@ Easton, Douglas F @@aut@@ Chenevix-Trench, Georgia @@aut@@ Antoniou, Antonis C @@aut@@ Mazoyer, Sylvie @@aut@@ Phelan, Catherine M @@aut@@ Sinilnikova, Olga M @@aut@@ Cox, David G @@aut@@ |
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This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Breast Cancer</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Breast Cancer Risk</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Mitochondrial Genome</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Mutation Carrier</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">BRCA2 Mutation</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" 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Blein, Sophie |
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Blein, Sophie misc Breast Cancer misc Breast Cancer Risk misc Mitochondrial Genome misc Mutation Carrier misc BRCA2 Mutation An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers |
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An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers Breast Cancer (dpeaa)DE-He213 Breast Cancer Risk (dpeaa)DE-He213 Mitochondrial Genome (dpeaa)DE-He213 Mutation Carrier (dpeaa)DE-He213 BRCA2 Mutation (dpeaa)DE-He213 |
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An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers |
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An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers |
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Blein, Sophie Bardel, Claire Danjean, Vincent McGuffog, Lesley Healey, Sue Barrowdale, Daniel Lee, Andrew Dennis, Joe Kuchenbaecker, Karoline B Soucy, Penny Terry, Mary Beth Chung, Wendy K Goldgar, David E Buys, Saundra S Janavicius, Ramunas Tihomirova, Laima Tung, Nadine Dorfling, Cecilia M van Rensburg, Elizabeth J Neuhausen, Susan L Ding, Yuan Chun Gerdes, Anne-Marie Ejlertsen, Bent Nielsen, Finn C Hansen, Thomas VO Osorio, Ana Benitez, Javier Conejero, Raquel Andrés Segota, Ena Weitzel, Jeffrey N Thelander, Margo Peterlongo, Paolo Radice, Paolo Pensotti, Valeria Dolcetti, Riccardo Bonanni, Bernardo Peissel, Bernard Zaffaroni, Daniela Scuvera, Giulietta Manoukian, Siranoush Varesco, Liliana Capone, Gabriele L Papi, Laura Ottini, Laura Yannoukakos, Drakoulis Konstantopoulou, Irene Garber, Judy Hamann, Ute Donaldson, Alan Brady, Angela Brewer, Carole Foo, Claire Evans, D Gareth Frost, Debra Eccles, Diana Douglas, Fiona Cook, Jackie Adlard, Julian Barwell, Julian Walker, Lisa Izatt, Louise Side, Lucy E Kennedy, M John Tischkowitz, Marc Rogers, Mark T Porteous, Mary E Morrison, Patrick J Platte, Radka Eeles, Ros Davidson, Rosemarie Hodgson, Shirley Cole, Trevor Godwin, Andrew K Isaacs, Claudine Claes, Kathleen De Leeneer, Kim Meindl, Alfons Gehrig, Andrea Wappenschmidt, Barbara Sutter, Christian Engel, Christoph Niederacher, Dieter Steinemann, Doris Plendl, Hansjoerg Kast, Karin Rhiem, Kerstin Ditsch, Nina Arnold, Norbert Varon-Mateeva, Raymonda Schmutzler, Rita K Preisler-Adams, Sabine Markov, Nadja Bogdanova Wang-Gohrke, Shan de Pauw, Antoine Lefol, Cédrick Lasset, Christine Leroux, Dominique Rouleau, Etienne Damiola, Francesca Dreyfus, Hélène Barjhoux, Laure Golmard, Lisa Uhrhammer, Nancy Bonadona, Valérie Sornin, Valérie Bignon, Yves-Jean Carter, Jonathan Van Le, Linda Piedmonte, Marion DiSilvestro, Paul A de la Hoya, Miguel Caldes, Trinidad Nevanlinna, Heli Aittomäki, Kristiina Jager, Agnes van den Ouweland, Ans MW Kets, Carolien M Aalfs, Cora M van Leeuwen, Flora E Hogervorst, Frans BL Meijers-Heijboer, Hanne EJ Oosterwijk, Jan C van Roozendaal, Kees EP Rookus, Matti A Devilee, Peter van der Luijt, Rob B Olah, Edith Diez, Orland Teulé, Alex Lazaro, Conxi Blanco, Ignacio Del Valle, Jesús Jakubowska, Anna Sukiennicki, Grzegorz Gronwald, Jacek Lubinski, Jan Durda, Katarzyna Jaworska-Bieniek, Katarzyna Agnarsson, Bjarni A Maugard, Christine Amadori, Alberto Montagna, Marco Teixeira, Manuel R Spurdle, Amanda B Foulkes, William Olswold, Curtis Lindor, Noralane M Pankratz, Vernon S Szabo, Csilla I Lincoln, Anne Jacobs, Lauren Corines, Marina Robson, Mark Vijai, Joseph Berger, Andreas Fink-Retter, Anneliese Singer, Christian F Rappaport, Christine Kaulich, Daphne Geschwantler Pfeiler, Georg Tea, Muy-Kheng Greene, Mark H Mai, Phuong L Rennert, Gad Imyanitov, Evgeny N Mulligan, Anna Marie Glendon, Gord Andrulis, Irene L Tchatchou, Sandrine Toland, Amanda Ewart Pedersen, Inge Sokilde Thomassen, Mads Kruse, Torben A Jensen, Uffe Birk Caligo, Maria A Friedman, Eitan Zidan, Jamal Laitman, Yael Lindblom, Annika Melin, Beatrice Arver, Brita Loman, Niklas Rosenquist, Richard Olopade, Olufunmilayo I Nussbaum, Robert L Ramus, Susan J Nathanson, Katherine L Domchek, Susan M Rebbeck, Timothy R Arun, Banu K Mitchell, Gillian Karlan, Beth Y Lester, Jenny Orsulic, Sandra Stoppa-Lyonnet, Dominique Thomas, Gilles Simard, Jacques Couch, Fergus J Offit, Kenneth Easton, Douglas F Chenevix-Trench, Georgia Antoniou, Antonis C Mazoyer, Sylvie Phelan, Catherine M Sinilnikova, Olga M Cox, David G |
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17 |
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Elektronische Aufsätze |
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Blein, Sophie |
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10.1186/s13058-015-0567-2 |
| title_sort |
original phylogenetic approach identified mitochondrial haplogroup t1a1 as inversely associated with breast cancer risk in brca2 mutation carriers |
| title_auth |
An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers |
| abstract |
Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects. © Blein et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstractGer |
Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects. © Blein et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstract_unstemmed |
Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects. © Blein et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers |
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Bardel, Claire Danjean, Vincent McGuffog, Lesley Healey, Sue Barrowdale, Daniel Lee, Andrew Dennis, Joe Kuchenbaecker, Karoline B Soucy, Penny Terry, Mary Beth Chung, Wendy K Goldgar, David E Buys, Saundra S Janavicius, Ramunas Tihomirova, Laima Tung, Nadine Dorfling, Cecilia M van Rensburg, Elizabeth J Neuhausen, Susan L Ding, Yuan Chun Gerdes, Anne-Marie Ejlertsen, Bent Nielsen, Finn C Hansen, Thomas VO Osorio, Ana Benitez, Javier Conejero, Raquel Andrés Segota, Ena Weitzel, Jeffrey N Thelander, Margo Peterlongo, Paolo Radice, Paolo Pensotti, Valeria Dolcetti, Riccardo Bonanni, Bernardo Peissel, Bernard Zaffaroni, Daniela Scuvera, Giulietta Manoukian, Siranoush Varesco, Liliana Capone, Gabriele L Papi, Laura Ottini, Laura Yannoukakos, Drakoulis Konstantopoulou, Irene Garber, Judy Hamann, Ute Donaldson, Alan Brady, Angela Brewer, Carole Foo, Claire Evans, D Gareth Frost, Debra Eccles, Diana Douglas, Fiona Cook, Jackie Adlard, Julian Barwell, Julian Walker, Lisa Izatt, Louise Side, Lucy E Kennedy, M John Tischkowitz, Marc Rogers, Mark T Porteous, Mary E Morrison, Patrick J Platte, Radka Eeles, Ros Davidson, Rosemarie Hodgson, Shirley Cole, Trevor Godwin, Andrew K Isaacs, Claudine Claes, Kathleen De Leeneer, Kim Meindl, Alfons Gehrig, Andrea Wappenschmidt, Barbara Sutter, Christian Engel, Christoph Niederacher, Dieter Steinemann, Doris Plendl, Hansjoerg Kast, Karin Rhiem, Kerstin Ditsch, Nina Arnold, Norbert Varon-Mateeva, Raymonda Schmutzler, Rita K Preisler-Adams, Sabine Markov, Nadja Bogdanova Wang-Gohrke, Shan de Pauw, Antoine Lefol, Cédrick Lasset, Christine Leroux, Dominique Rouleau, Etienne Damiola, Francesca Dreyfus, Hélène Barjhoux, Laure Golmard, Lisa Uhrhammer, Nancy Bonadona, Valérie Sornin, Valérie Bignon, Yves-Jean Carter, Jonathan Van Le, Linda Piedmonte, Marion DiSilvestro, Paul A de la Hoya, Miguel Caldes, Trinidad Nevanlinna, Heli Aittomäki, Kristiina Jager, Agnes van den Ouweland, Ans MW Kets, Carolien M Aalfs, Cora M van Leeuwen, Flora E Hogervorst, Frans BL Meijers-Heijboer, Hanne EJ Oosterwijk, Jan C van Roozendaal, Kees EP Rookus, Matti A Devilee, Peter van der Luijt, Rob B Olah, Edith Diez, Orland Teulé, Alex Lazaro, Conxi Blanco, Ignacio Del Valle, Jesús Jakubowska, Anna Sukiennicki, Grzegorz Gronwald, Jacek Lubinski, Jan Durda, Katarzyna Jaworska-Bieniek, Katarzyna Agnarsson, Bjarni A Maugard, Christine Amadori, Alberto Montagna, Marco Teixeira, Manuel R Spurdle, Amanda B Foulkes, William Olswold, Curtis Lindor, Noralane M Pankratz, Vernon S Szabo, Csilla I Lincoln, Anne Jacobs, Lauren Corines, Marina Robson, Mark Vijai, Joseph Berger, Andreas Fink-Retter, Anneliese Singer, Christian F Rappaport, Christine Kaulich, Daphne Geschwantler Pfeiler, Georg Tea, Muy-Kheng Greene, Mark H Mai, Phuong L Rennert, Gad Imyanitov, Evgeny N Mulligan, Anna Marie Glendon, Gord Andrulis, Irene L Tchatchou, Sandrine Toland, Amanda Ewart Pedersen, Inge Sokilde Thomassen, Mads Kruse, Torben A Jensen, Uffe Birk Caligo, Maria A Friedman, Eitan Zidan, Jamal Laitman, Yael Lindblom, Annika Melin, Beatrice Arver, Brita Loman, Niklas Rosenquist, Richard Olopade, Olufunmilayo I Nussbaum, Robert L Ramus, Susan J Nathanson, Katherine L Domchek, Susan M Rebbeck, Timothy R Arun, Banu K Mitchell, Gillian Karlan, Beth Y Lester, Jenny Orsulic, Sandra Stoppa-Lyonnet, Dominique Thomas, Gilles Simard, Jacques Couch, Fergus J Offit, Kenneth Easton, Douglas F Chenevix-Trench, Georgia Antoniou, Antonis C Mazoyer, Sylvie Phelan, Catherine M Sinilnikova, Olga M Cox, David G |
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Bardel, Claire Danjean, Vincent McGuffog, Lesley Healey, Sue Barrowdale, Daniel Lee, Andrew Dennis, Joe Kuchenbaecker, Karoline B Soucy, Penny Terry, Mary Beth Chung, Wendy K Goldgar, David E Buys, Saundra S Janavicius, Ramunas Tihomirova, Laima Tung, Nadine Dorfling, Cecilia M van Rensburg, Elizabeth J Neuhausen, Susan L Ding, Yuan Chun Gerdes, Anne-Marie Ejlertsen, Bent Nielsen, Finn C Hansen, Thomas VO Osorio, Ana Benitez, Javier Conejero, Raquel Andrés Segota, Ena Weitzel, Jeffrey N Thelander, Margo Peterlongo, Paolo Radice, Paolo Pensotti, Valeria Dolcetti, Riccardo Bonanni, Bernardo Peissel, Bernard Zaffaroni, Daniela Scuvera, Giulietta Manoukian, Siranoush Varesco, Liliana Capone, Gabriele L Papi, Laura Ottini, Laura Yannoukakos, Drakoulis Konstantopoulou, Irene Garber, Judy Hamann, Ute Donaldson, Alan Brady, Angela Brewer, Carole Foo, Claire Evans, D Gareth Frost, Debra Eccles, Diana Douglas, Fiona Cook, Jackie Adlard, Julian Barwell, Julian Walker, Lisa Izatt, Louise Side, Lucy E Kennedy, M John Tischkowitz, Marc Rogers, Mark T Porteous, Mary E Morrison, Patrick J Platte, Radka Eeles, Ros Davidson, Rosemarie Hodgson, Shirley Cole, Trevor Godwin, Andrew K Isaacs, Claudine Claes, Kathleen De Leeneer, Kim Meindl, Alfons Gehrig, Andrea Wappenschmidt, Barbara Sutter, Christian Engel, Christoph Niederacher, Dieter Steinemann, Doris Plendl, Hansjoerg Kast, Karin Rhiem, Kerstin Ditsch, Nina Arnold, Norbert Varon-Mateeva, Raymonda Schmutzler, Rita K Preisler-Adams, Sabine Markov, Nadja Bogdanova Wang-Gohrke, Shan de Pauw, Antoine Lefol, Cédrick Lasset, Christine Leroux, Dominique Rouleau, Etienne Damiola, Francesca Dreyfus, Hélène Barjhoux, Laure Golmard, Lisa Uhrhammer, Nancy Bonadona, Valérie Sornin, Valérie Bignon, Yves-Jean Carter, Jonathan Van Le, Linda Piedmonte, Marion DiSilvestro, Paul A de la Hoya, Miguel Caldes, Trinidad Nevanlinna, Heli Aittomäki, Kristiina Jager, Agnes van den Ouweland, Ans MW Kets, Carolien M Aalfs, Cora M van Leeuwen, Flora E Hogervorst, Frans BL Meijers-Heijboer, Hanne EJ Oosterwijk, Jan C van Roozendaal, Kees EP Rookus, Matti A Devilee, Peter van der Luijt, Rob B Olah, Edith Diez, Orland Teulé, Alex Lazaro, Conxi Blanco, Ignacio Del Valle, Jesús Jakubowska, Anna Sukiennicki, Grzegorz Gronwald, Jacek Lubinski, Jan Durda, Katarzyna Jaworska-Bieniek, Katarzyna Agnarsson, Bjarni A Maugard, Christine Amadori, Alberto Montagna, Marco Teixeira, Manuel R Spurdle, Amanda B Foulkes, William Olswold, Curtis Lindor, Noralane M Pankratz, Vernon S Szabo, Csilla I Lincoln, Anne Jacobs, Lauren Corines, Marina Robson, Mark Vijai, Joseph Berger, Andreas Fink-Retter, Anneliese Singer, Christian F Rappaport, Christine Kaulich, Daphne Geschwantler Pfeiler, Georg Tea, Muy-Kheng Greene, Mark H Mai, Phuong L Rennert, Gad Imyanitov, Evgeny N Mulligan, Anna Marie Glendon, Gord Andrulis, Irene L Tchatchou, Sandrine Toland, Amanda Ewart Pedersen, Inge Sokilde Thomassen, Mads Kruse, Torben A Jensen, Uffe Birk Caligo, Maria A Friedman, Eitan Zidan, Jamal Laitman, Yael Lindblom, Annika Melin, Beatrice Arver, Brita Loman, Niklas Rosenquist, Richard Olopade, Olufunmilayo I Nussbaum, Robert L Ramus, Susan J Nathanson, Katherine L Domchek, Susan M Rebbeck, Timothy R Arun, Banu K Mitchell, Gillian Karlan, Beth Y Lester, Jenny Orsulic, Sandra Stoppa-Lyonnet, Dominique Thomas, Gilles Simard, Jacques Couch, Fergus J Offit, Kenneth Easton, Douglas F Chenevix-Trench, Georgia Antoniou, Antonis C Mazoyer, Sylvie Phelan, Catherine M Sinilnikova, Olga M Cox, David G |
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This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Introduction Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. 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| score |
7.399617 |