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Abstract:
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Many genome-wide association studies, in which 100,000s of SNPs are genotyped in studies with a few thousand participants are now being carried out. Some initial successes have been reported. Most of these results have come from single SNP analyses. It is generally assumed that many genes (SNPs) contribute jointly, either additively or with epistatic effects, to the risk if disease. Clearly because of the size of the problem it is harder to identify epistatic effects. In this talk we will discuss approaches to increase the power to identify such effects, as well as methods to combine significant single SNPs and identified epistatic effects to form genetic risk models.
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