TY - JOUR A1 - Blein, Sophie A1 - Bardel, Claire A1 - Danjean, Vincent A1 - McGuffog, Lesley A1 - Healay, Sue A1 - Barrowdale, Daniel A1 - Lee, Andrew A1 - Dennis, Joe A1 - Kuchenbaecker, Karoline B. A1 - Soucy, Penny A1 - Terry, Mary Beth A1 - Chung, Wendy K. A1 - Goldgar, David E. A1 - Buys, Saundra S. A1 - Janavicius, Ramunas A1 - Tihomirova, Laima A1 - Tung, Nadine A1 - Dorfling, Cecilia M. A1 - van Rensburg, Elizabeth J. A1 - Neuhausen, Susan L. A1 - Ding, Yuan Chun A1 - Gerdes, Anne-Marie A1 - Ejlertsen, Bent A1 - Nielsen, Finn C. A1 - Hansen, Thomas V. O. A1 - Osorio, Ana A1 - Benitez, Javier A1 - Andreas Conejero, Raquel A1 - Segota, Ena A1 - Weitzel, Jeffrey N. A1 - Thelander, Margo A1 - Peterlongo, Paolo A1 - Radice, Paolo A1 - Pensotti, Valeria A1 - Dolcetti, Riccardo A1 - Bonanni, Bernardo A1 - Peissel, Bernard A1 - Zaffaroni, Daniela A1 - Scuvera, Giulietta A1 - Manoukian, Siranoush A1 - Varesco, Liliana A1 - Capone, Gabriele L. A1 - Papi, Laura A1 - Ottini, Laura A1 - Yannoukakos, Drakoulis A1 - Konstantopoulou, Irene A1 - Garber, Judy A1 - Hamann, Ute A1 - Donaldson, Alan A1 - Brady, Angela A1 - Brewer, Carole A1 - Foo, Claire A1 - Evans, D. Gareth A1 - Frost, Debra A1 - Eccles, Diana A1 - Douglas, Fiona A1 - Cook, Jackie A1 - Adlard, Julian A1 - Barwell, Julian A1 - Walker, Lisa A1 - Izatt, Louise A1 - Side, Lucy E. A1 - Kennedy, M. John A1 - Tischkowitz, Marc A1 - Rogers, Mark T. A1 - Porteous, Mary E. A1 - Morrison, Patrick J. A1 - Platte, Radka A1 - Eeles, Ros A1 - Davidson, Rosemarie A1 - Hodgson, Shirley A1 - Cole, Trevor A1 - Godwin, Andrew K A1 - Isaacs, Claudine A1 - Claes, Kathleen A1 - De Leeneer, Kim A1 - Meindl, Alfons A1 - Gehrig, Andrea A1 - Wappenschmidt, Barbara A1 - Sutter, Christian A1 - Engel, Christoph A1 - Niederacher, Dieter A1 - Steinemann, Doris A1 - Plendl, Hansjoerg A1 - Kast, Karin A1 - Rhiem, Kerstin A1 - Ditsch, Nina A1 - Arnold, Norbert A1 - Varon-Mateeva, Raymonda A1 - Schmutzler, Rita K. A1 - Preisler-Adams, Sabine A1 - Markov, Nadja Bogdanova A1 - Wang-Gohrke, Shan A1 - de Pauw, Antoine A1 - Lefol, Cedrick A1 - Lasset, Christine A1 - Leroux, Dominique A1 - Rouleau, Etienne A1 - Damiola, Francesca A1 - Dreyfus, Helene A1 - Barjhoux, Laure A1 - Golmard, Lisa A1 - Uhrhammer, Nancy A1 - Bonadona, Valerie A1 - Sornin, Valerie A1 - Bignon, Yves-Jean A1 - Carter, Jonathan A1 - Van Le, Linda A1 - Piedmonte, Marion A1 - DiSilvestro, Paul A. A1 - de la Hoya, Miguel A1 - Caldes, Trinidad A1 - Nevanlinna, Heli A1 - Aittomäki, Kristiina A1 - Jager, Agnes A1 - van den Ouweland, Ans M. W. A1 - Kets, Carolien M. A1 - Aalfs, Cora M. A1 - van Leeuwen, Flora E. A1 - Hogervorst, Frans B. L. A1 - Meijers-Heijboer, Hanne E. J. A1 - Oosterwijk, Jan C. A1 - van Roozendaal, Kees E. P. A1 - Rookus, Matti A. A1 - Devilee, Peter A1 - van der Luijt, Rob B. A1 - Olah, Edith A1 - Diez, Orland A1 - Teule, Alex A1 - Lazaro, Conxi A1 - Blanco, Ignacio A1 - Del Valle, Jesus A1 - Jakubowska, Anna A1 - Sukiennicki, Grzegorz A1 - Gronwald, Jacek A1 - Spurdle, Amanda B. A1 - Foulkes, William A1 - Olswold, Curtis A1 - Lindor, Noralene M. A1 - Pankratz, Vernon S. A1 - Szabo, Csilla I. A1 - Lincoln, Anne A1 - Jacobs, Lauren A1 - Corines, Marina A1 - Robson, Mark A1 - Vijai, Joseph A1 - Berger, Andreas A1 - Fink-Retter, Anneliese A1 - Singer, Christian F. A1 - Rappaport, Christine A1 - Geschwantler Kaulich, Daphne A1 - Pfeiler, Georg A1 - Tea, Muy-Kheng A1 - Greene, Mark H. A1 - Mai, Phuong L. A1 - Rennert, Gad A1 - Imyanitov, Evgeny N. A1 - Mulligan, Anna Marie A1 - Glendon, Gord A1 - Andrulis, Irene L. A1 - Tchatchou, Andrine A1 - Toland, Amanda Ewart A1 - Pedersen, Inge Sokilde A1 - Thomassen, Mads A1 - Kruse, Torben A. A1 - Jensen, Uffe Birk A1 - Caligo, Maria A. A1 - Friedman, Eitan A1 - Zidan, Jamal A1 - Laitman, Yael A1 - Lindblom, Annika A1 - Melin, Beatrice A1 - Arver, Brita A1 - Loman, Niklas A1 - Rosenquist, Richard A1 - Olopade, Olufunmilayo I. A1 - Nussbaum, Robert L. A1 - Ramus, Susan J. A1 - Nathanson, Katherine L. A1 - Domchek, Susan M. A1 - Rebbeck, Timothy R. A1 - Arun, Banu K. A1 - Mitchell, Gillian A1 - Karlan, Bethy Y. A1 - Lester, Jenny A1 - Orsulic, Sandra A1 - Stoppa-Lyonnet, Dominique A1 - Thomas, Gilles A1 - Simard, Jacques A1 - Couch, Fergus J. A1 - Offit, Kenenth A1 - Easton, Douglas F. A1 - Chenevix-Trench, Georgia A1 - Antoniou, Antonis C. A1 - Mazoyer, Sylvie A1 - Phelan, Catherine M. A1 - Sinilnikova, Olga M. A1 - Cox, David G. T1 - An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers JF - Breast Cancer Research N2 - 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. KW - single-nucleotide polymorphisms KW - genetic modifiers KW - oxidative stress KW - consortium KW - multiple diseases KW - DNA KW - haplogroups KW - susceptibility KW - Ovarian KW - variants Y1 - 2015 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-145458 VL - 17 IS - 61 ER - TY - JOUR A1 - Biedermann, Benedikt A1 - Denner, Ansgar A1 - Dittmaier, Stefan A1 - Hofer, Lars A1 - Jäger, Barbara T1 - Next-to-leading-order electroweak corrections to the production of four charged leptons at the LHC JF - Journal of High Energy Physics N2 - We present a state-of-the-art calculation of the next-to leading-order electroweak corrections to ZZ production, including the leptonic decays of the Z bosons into μ\(^+\)μ\(^ −\)e\(^+\)e\(^−\) or μ\(^+\)μ\(^−\)μ\(^+\)μ\(^−\) final states. We use complete leading-order and next-to-leading-order matrix elements for four-lepton production, including contributions of virtual photons and all off-shell effects of Z bosons, where the finite Z-boson width is taken into account using the complex-mass scheme. The matrix elements are implemented into Monte Carlo programs allowing for the evaluation of arbitrary differential distributions. We present integrated and differential cross sections for the LHC at 13 TeV both for an inclusive setup where only lepton identification cuts are applied, and for a setup motivated by Higgs-boson analyses in the four-lepton decay channel. The electroweak corrections are divided into photonic and purely weak contributions. The former show the well-known pronounced tails near kinematical thresholds and resonances; the latter are generically at the level of ∼ −5% and reach several −10% in the high-energy tails of distributions. Comparing the results for μ\(^+\)μ\(^−\)e\(^+\)e\(^−\) and μ\(^+\)μ\(^−\)μ\(^+\)μ\(^−\) final states, we find significant differences mainly in distributions that are sensitive to the μ\(^+\)μ\(^−\) pairing in the μ\(^+\)μ\(^−\)μ\(^+\)μ\(^−\) final state. Differences between μ\(^+\)μ\(^−\)e\(^+\)e\(^−\) and μ\(^+\)μ\(^−\)μ\(^+\)μ\(^−\) channels due to interferences of equal-flavour leptons in the final state can reach up to 10% in off-shell-sensitive regions. Contributions induced by incoming photons, i.e. photon-photon and quark-photon channels, are included, but turn out to be phenomenologically unimportant. KW - physics KW - NLO Computations Y1 - 2017 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-171966 IS - 1 ER -