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Breast cancer exhibits familial aggregation, consistent with variation in genetic susceptibility to the disease. Known susceptibility genes account for less than 25% of the familial risk of breast cancer, and the residual genetic variance is likely to be due to variants conferring more moderate risks. To identify further susceptibility alleles, we conducted a two-stage genome-wide association study in 4,398 breast cancer cases and 4,316 controls, followed by a third stage in which 30 single nucleotide polymorphisms (SNPs) were tested for confirmation in 21,860 cases and 22,578 controls from 22 studies. We used 227,876 SNPs that were estimated to correlate with 77% of known common SNPs in Europeans at r2 > 0.5. SNPs in five novel independent loci exhibited strong and consistent evidence of association with breast cancer (P < 10(-7)). Four of these contain plausible causative genes (FGFR2, TNRC9, MAP3K1 and LSP1). At the second stage, 1,792 SNPs were significant at the P < 0.05 level compared with an estimated 1,343 that would be expected by chance, indicating that many additional common susceptibility alleles may be identifiable by this approach.

Original publication

DOI

10.1038/nature05887

Type

Journal article

Journal

Nature

Publication Date

06/2007

Volume

447

Pages

1087 - 1093

Addresses

CR-UK Genetic Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge CB1 8RN, UK. d.easton@srl.cam.ac.uk

Keywords

SEARCH collaborators, kConFab, AOCS Management Group, Humans, Breast Neoplasms, Genetic Predisposition to Disease, Microfilament Proteins, MAP Kinase Kinase Kinase 1, Receptors, Progesterone, Odds Ratio, Case-Control Studies, Genotype, Polymorphism, Single Nucleotide, Alleles, Genome, Human, North America, Asia, Southeastern, Australia, Europe, Female, Receptor, Fibroblast Growth Factor, Type 2