Browsing by Author "Foretova, L"
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McKay, James D.; Truong, Therese; Gaborieau, V; Chabrier, Amelie; Chuang, Shu-Chun; Byrnes, G; Zaridze, D; Shangina, O; Szeszenia-Dabrowska, N; Lissowska, Jolanta; Rudnai, P; Fabianova, E; Bucur, A; Bencko, V; Holcatova, I; Janout, V; Foretova, L; Lagiou, Pagona; Trichopoulos, Dimitrios; Benhamou, S; Ahrens, Wolfgang; Bouchardy, C; Merletti, F; Richiardi, L; Talamini, R; Simonato, L; Barzan, L; Kjærheim, Kristina; Macfarlane, G; Agudo, Antonio; Macfarlane, Tatiana V.; Canova, C; Castellsague, X; Conway, DI; Lowry, R; Healy, CM; McKinney, PA; Toner, ME; Znaor, A; Menezes, A; Curado, MP; Koifman, S; Neto, JE; Wünsch-Filho, V; Boccia, S; Arzani, D; Garrote, LF; Cadoni, G; Olshan, AF; Weissler, MC; Luo, JC; Funkhouser, WK; Lubinski, Jan; Lener, M; Trubicka, J; Schwartz, SM; Oszutowska, D; Doody, DR; Chen, C; Fish, S; Lazarus, P; Muscat, JE; Gallagher, CJ; Zhang, Zuo-Feng; Chang, SC; Wei, QY; Sturgis, EM; Franceschi, S; Kelsey, KT; Wang, LE; Herrero, R; Marsit, CJ; McClean, MD; Romkes, M; Nelson, HH; Buch, S; Nukui, T; Zhong, SL; Lacko, M; Manni, JJ; McLaughlin, J; Hung, RJ; Peters, WHM; Vatten, Lars Johan; Njølstad, Inger; Goodman, GE; Field, JK; Palli, D; Liloglou, T; Clavel-Chapelon, F; Vineis, P; Krogh, V; Tumino, R; Panico, S; Martinez, Carmen; Gonzalez, CA; Quiros, JR; Navarro, C; Larranaga, N; Khaw, KT; Ardanaz, E; Key, T; Peeters, PHM; Bueno-De-Mesquita, HB; Boeing, H; Overvad, K; Trichopoulou, A; Linseisen, J; Hallmans, G; Tjønneland, Anne; Riboli, Elio; Kumle, Merethe; Valk, K; Voodern, Tonu; Metspalu, Andres; Boland, A; Zelenika, D; Delepine, M; Foglio, M; Lechner, D; Blanché, Hélène; Gut, Ivo G.; Galan, P; Hashibe, Mia; Heath, Simon; Hayes, Richard B.; Lathrop, Mark; Boffetta, Paolo; Brennan, Paul (Journal article; Tidsskriftartikkel; Peer reviewed, 2011)[+][-]
Abstract: Genome-wide association studies (GWAS) have been successful in identifying common genetic variation involved in susceptibility to etiologically complex disease. We conducted a GWAS to identify common genetic variation involved in susceptibility to upper aero-digestive tract (UADT) cancers. Genome-wide genotyping was carried out using the Illumina HumanHap300 beadchips in 2,091 UADT cancer cases and 3,513 controls from two large European multi-centre UADT cancer studies, as well as 4,821 generic controls. The 19 top-ranked variants were investigated further in an additional 6,514 UADT cancer cases and 7,892 controls of European descent from an additional 13 UADT cancer studies participating in the INHANCE consortium. Five common variants presented evidence for significant association in the combined analysis (p≤5×10−7). Two novel variants were identified, a 4q21 variant (rs1494961, p = 1×10−8) located near DNA repair related genes HEL308 and FAM175A (or Abraxas) and a 12q24 variant (rs4767364, p = 2×10−8) located in an extended linkage disequilibrium region that contains multiple genes including the aldehyde dehydrogenase 2 (ALDH2) gene. Three remaining variants are located in the ADH gene cluster and were identified previously in a candidate gene study involving some of these samples. The association between these three variants and UADT cancers was independently replicated in 5,092 UADT cancer cases and 6,794 controls non-overlapping samples presented here (rs1573496-ADH7, p = 5×10−8; rs1229984-ADH1B, p = 7×10−9; and rs698-ADH1C, p = 0.02). These results implicate two variants at 4q21 and 12q24 and further highlight three ADH variants in UADT cancer susceptibility. URI: http://hdl.handle.net/10037/4033 File(s) in this item: 1
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Timofeeva, MN; Hung, RJ; Rafnar, T; Christiani, DC; Field, JK; Bickeboller, H; Risch, A; McKay, JD; Wang, Y; Dai, J; Gaborieau, V; McLaughlin, J; Brenner, D; Narod, SA; Caporaso, NE.; Albanes, D; Thun, M; Eisen, T; Wichmann, HE; Rosenberger, A; Han, Y; Chen, W; Zhu, D; Spitz, M; Wu, X; Pande, M; Zhao, Y; Zaridze, D; Szeszenia-Dabrowska, N; Lissowska, J; Rudnai, P; Fabianova, E; Mates, D; Bencko, V; Foretova, L; Janout, V; Krokan, Hans Einar; Gabrielsen, Maiken Elvestad; Skorpen, Frank; Vatten, Lars Johan; Njølstad, Inger; Chen, C; Goodman, G; Lathrop, M; Benhamou, S; Vooder, T; Valk, K; Nelis, M; Metspalu, Andres; Raji, O; Chen, Y; Gosney, J; Liloglou, T; Muley, T; Dienemann, H; Thorleifsson, G; Shen, H.; Stefansson, Kari; Brennan, Paul; Amos, CI; Houlston, Richard; Landi, MT (Journal article; Tidsskriftartikkel; Peer reviewed, 2012)[+][-]
Abstract: Recent genome-wide association studies (GWASs) have identified common genetic variants at 5p15.33, 6p21–6p22 and 15q25.1 associated with lung cancer risk. Several other genetic regions including variants of CHEK2 (22q12), TP53BP1 (15q15) and RAD52 (12p13) have been demonstrated to influence lung cancer risk in candidate- or pathway-based analyses. To identify novel risk variants for lung cancer, we performed a meta-analysis of 16 GWASs, totaling 14 900 cases and 29 485 controls of European descent. Our data provided increased support for previously identified risk loci at 5p15 (P = 7.2 × 10−16), 6p21 (P = 2.3 × 10−14) and 15q25 (P = 2.2 × 10−63). Furthermore, we demonstrated histology-specific effects for 5p15, 6p21 and 12p13 loci but not for the 15q25 region. Subgroup analysis also identified a novel disease locus for squamous cell carcinoma at 9p21 (CDKN2A/p16INK4A/p14ARF/CDKN2B/p15INK4B/ANRIL; rs1333040, P = 3.0 × 10−7) which was replicated in a series of 5415 Han Chinese (P = 0.03; combined analysis, P = 2.3 × 10−8). This large analysis provides additional evidence for the role of inherited genetic susceptibility to lung cancer and insight into biological differences in the development of the different histological types of lung cancer. URI: http://hdl.handle.net/10037/4972 File(s) in this item: 1
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