Résumé
Background:Breast cancer is one of the most common malignancies in women. Genome-wide association studies have identified FGFR2 as a breast cancer susceptibility gene. Common variation in other fibroblast growth factor (FGF) receptors might also modify risk. We tested this hypothesis by studying genotyped single-nucleotide polymorphisms (SNPs) and imputed SNPs in FGFR1, FGFR3, FGFR4 and FGFRL1 in the Breast Cancer Association Consortium.Methods:Data were combined from 49 studies, including 53 835 cases and 50 156 controls, of which 89 050 (46 450 cases and 42 600 controls) were of European ancestry, 12 893 (6269 cases and 6624 controls) of Asian and 2048 (1116 cases and 932 controls) of African ancestry. Associations with risk of breast cancer, overall and by disease sub-type, were assessed using unconditional logistic regression.Results:Little evidence of association with breast cancer risk was observed for SNPs in the FGF receptor genes. The strongest evidence in European women was for rs743682 in FGFR3; the estimated per-allele odds ratio was 1.05 (95% confidence interval=1.02-1.09, P=0.0020), which is substantially lower than that observed for SNPs in FGFR2.Conclusion:Our results suggest that common variants in the other FGF receptors are not associated with risk of breast cancer to the degree observed for FGFR2.
langue originale | Anglais |
---|---|
Pages (de - à) | 1088-1100 |
Nombre de pages | 13 |
journal | British Journal of Cancer |
Volume | 110 |
Numéro de publication | 4 |
Les DOIs | |
état | Publié - 18 févr. 2014 |
Modification externe | Oui |
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Dans: British Journal of Cancer, Vol 110, Numéro 4, 18.02.2014, p. 1088-1100.
Résultats de recherche: Contribution à un journal › Article › Revue par des pairs
TY - JOUR
T1 - FGF receptor genes and breast cancer susceptibility
T2 - Results from the Breast Cancer Association Consortium
AU - Agarwal, D.
AU - Pineda, S.
AU - Michailidou, K.
AU - Herranz, J.
AU - Pita, G.
AU - Moreno, L. T.
AU - Alonso, M. R.
AU - Dennis, J.
AU - Wang, Q.
AU - Bolla, M. K.
AU - Meyer, K. B.
AU - Menéndez-Rodríguez, P.
AU - Hardisson, D.
AU - Mendiola, M.
AU - González-Neira, A.
AU - Lindblom, A.
AU - Margolin, S.
AU - Swerdlow, A.
AU - Ashworth, A.
AU - Orr, N.
AU - Jones, M.
AU - Matsuo, K.
AU - Ito, H.
AU - Iwata, H.
AU - Kondo, N.
AU - Hartman, M.
AU - Hui, M.
AU - Lim, W. Y.
AU - Iau, P. T.C.
AU - Sawyer, E.
AU - Tomlinson, I.
AU - Kerin, M.
AU - Miller, N.
AU - Kang, D.
AU - Choi, J. Y.
AU - Park, S.
AU - Noh, D. Y.
AU - Hopper, J. L.
AU - Schmidt, D. F.
AU - Makalic, E.
AU - Southey, M. C.
AU - Teo, S. H.
AU - Yip, C. H.
AU - Sivanandan, K.
AU - Tay, W. T.
AU - Brauch, H.
AU - Brüning, T.
AU - Hamann, U.
AU - Dunning, A. M.
AU - Shah, M.
AU - Andrulis, I. L.
AU - Knight, J. A.
AU - Glendon, G.
AU - Tchatchou, S.
AU - Schmidt, M. K.
AU - Broeks, A.
AU - Rosenberg, E. H.
AU - van't Veer, L. J.
AU - Fasching, P. A.
AU - Renner, S. P.
AU - Ekici, A. B.
AU - Beckmann, M. W.
AU - Shen, C. Y.
AU - Hsiung, C. N.
AU - Yu, J. C.
AU - Hou, M. F.
AU - Blot, W.
AU - Cai, Q.
AU - Wu, A. H.
AU - Tseng, C. C.
AU - Van Den Berg, D.
AU - Stram, D. O.
AU - Cox, A.
AU - Brock, I. W.
AU - Reed, M. W.R.
AU - Muir, K.
AU - Lophatananon, A.
AU - Stewart-Brown, S.
AU - Siriwanarangsan, P.
AU - Zheng, W.
AU - Deming-Halverson, S.
AU - Shrubsole, M. J.
AU - Long, J.
AU - Shu, X. O.
AU - Lu, W.
AU - Gao, Y. T.
AU - Zhang, B.
AU - Radice, P.
AU - Peterlongo, P.
AU - Manoukian, S.
AU - Mariette, F.
AU - Sangrajrang, S.
AU - McKay, J.
AU - Couch, F. J.
AU - Toland, A. E.
AU - Yannoukakos, D.
AU - Fletcher, O.
AU - Johnson, N.
AU - Dos Santos Silva, I.
AU - Peto, J.
AU - Marme, F.
AU - Burwinkel, B.
AU - Guénel, P.
AU - Truong, T.
AU - Sanchez, M.
AU - Mulot, C.
AU - Bojesen, S. E.
AU - Nordestgaard, B. G.
AU - Flyer, H.
AU - Brenner, H.
AU - Dieffenbach, A. K.
AU - Arndt, V.
AU - Stegmaier, C.
AU - Mannermaa, A.
AU - Kataja, V.
AU - Kosma, V. M.
AU - Hartikainen, J. M.
AU - Lambrechts, D.
AU - Yesilyurt, B. T.
AU - Floris, G.
AU - Leunen, K.
AU - Chang-Claude, J.
AU - Rudolph, A.
AU - Seibold, P.
AU - Flesch-Janys, D.
AU - Wang, X.
AU - Olson, J. E.
AU - Vachon, C.
AU - Purrington, K.
AU - Giles, G. G.
AU - Severi, G.
AU - Baglietto, L.
AU - Haiman, C. A.
AU - Henderson, B. E.
AU - Schumacher, F.
AU - Le Marchand, L.
AU - Simard, J.
AU - Dumont, M.
AU - Goldberg, M. S.
AU - Labrèche, F.
AU - Winqvist, R.
AU - Pylkäs, K.
AU - Jukkola-Vuorinen, A.
AU - Grip, M.
AU - Devilee, P.
AU - E M Tollenaar, R. A.
AU - Seynaeve, C.
AU - García-Closas, M.
AU - Chanock, S. J.
AU - Lissowska, J.
AU - Figueroa, J. D.
AU - Czene, K.
AU - Eriksson, M.
AU - Humphreys, K.
AU - Darabi, H.
AU - Hooning, M. J.
AU - Kriege, M.
AU - Collée, J. M.
AU - Tilanus-Linthorst, M.
AU - Li, J.
AU - Jakubowska, A.
AU - Lubinski, J.
AU - Jaworska-Bieniek, K.
AU - Durda, K.
AU - Nevanlinna, H.
AU - Muranen, T. A.
AU - Aittomäki, K.
AU - Blomqvist, C.
AU - Bogdanova, N.
AU - Dörk, T.
AU - Hall, P.
AU - Chenevix-Trench, G.
AU - Easton, D. F.
AU - P Pharoah, P. D.
AU - Arias-Perez, J. I.
AU - Zamora, P.
AU - Benítez, J.
AU - Milne, R. L.
PY - 2014/2/18
Y1 - 2014/2/18
N2 - Background:Breast cancer is one of the most common malignancies in women. Genome-wide association studies have identified FGFR2 as a breast cancer susceptibility gene. Common variation in other fibroblast growth factor (FGF) receptors might also modify risk. We tested this hypothesis by studying genotyped single-nucleotide polymorphisms (SNPs) and imputed SNPs in FGFR1, FGFR3, FGFR4 and FGFRL1 in the Breast Cancer Association Consortium.Methods:Data were combined from 49 studies, including 53 835 cases and 50 156 controls, of which 89 050 (46 450 cases and 42 600 controls) were of European ancestry, 12 893 (6269 cases and 6624 controls) of Asian and 2048 (1116 cases and 932 controls) of African ancestry. Associations with risk of breast cancer, overall and by disease sub-type, were assessed using unconditional logistic regression.Results:Little evidence of association with breast cancer risk was observed for SNPs in the FGF receptor genes. The strongest evidence in European women was for rs743682 in FGFR3; the estimated per-allele odds ratio was 1.05 (95% confidence interval=1.02-1.09, P=0.0020), which is substantially lower than that observed for SNPs in FGFR2.Conclusion:Our results suggest that common variants in the other FGF receptors are not associated with risk of breast cancer to the degree observed for FGFR2.
AB - Background:Breast cancer is one of the most common malignancies in women. Genome-wide association studies have identified FGFR2 as a breast cancer susceptibility gene. Common variation in other fibroblast growth factor (FGF) receptors might also modify risk. We tested this hypothesis by studying genotyped single-nucleotide polymorphisms (SNPs) and imputed SNPs in FGFR1, FGFR3, FGFR4 and FGFRL1 in the Breast Cancer Association Consortium.Methods:Data were combined from 49 studies, including 53 835 cases and 50 156 controls, of which 89 050 (46 450 cases and 42 600 controls) were of European ancestry, 12 893 (6269 cases and 6624 controls) of Asian and 2048 (1116 cases and 932 controls) of African ancestry. Associations with risk of breast cancer, overall and by disease sub-type, were assessed using unconditional logistic regression.Results:Little evidence of association with breast cancer risk was observed for SNPs in the FGF receptor genes. The strongest evidence in European women was for rs743682 in FGFR3; the estimated per-allele odds ratio was 1.05 (95% confidence interval=1.02-1.09, P=0.0020), which is substantially lower than that observed for SNPs in FGFR2.Conclusion:Our results suggest that common variants in the other FGF receptors are not associated with risk of breast cancer to the degree observed for FGFR2.
UR - http://www.scopus.com/inward/record.url?scp=84894304619&partnerID=8YFLogxK
U2 - 10.1038/bjc.2013.769
DO - 10.1038/bjc.2013.769
M3 - Article
C2 - 24548884
AN - SCOPUS:84894304619
SN - 0007-0920
VL - 110
SP - 1088
EP - 1100
JO - British Journal of Cancer
JF - British Journal of Cancer
IS - 4
ER -