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An alternative approach is to use hypothesis-driven association studies of specific asthma candidate genes.11,12 This is most commonly performed using a case�Ccontrol design although cohort and family-based approaches are possible. However, Oxacillin there has also been a general lack of reproducibility in these types of studies.13 There are many possible reasons for such inconsistent results and these include small sample sizes, differences in phenotype definition and lack of adequate matching of study subjects for ethnic background.14 However, it is also possible that different populations have different genetic risk alleles and the lack of replication simply reflects the genetic heterogeneity underlying the asthma phenotype. In addition, environmental factors are clearly important in the pathogenesis of asthma and gene by environment interactions are infrequently included in genetic studies. A factor that has to be taken into consideration in association studies is the phenomenon of linkage disequilibrium (LD), which is the association between alleles at different sites on a chromosome. LD tends to be lower for polymorphisms that are further apart (due to the effect of recombination), although there is not a simple relationship between LD and genetic distance. The pattern of LD across the genome is not uniform and differs between populations of different ancestry. As a consequence of LD, an association of a genetic polymorphism with a disease outcome does not necessarily imply causality. The polymorphism may be in LD with several nearby variants, any one of which could be the EPZ5676 in vivo causal locus. On the other hand, the presence of LD reduces the number of polymorphisms that have to be assayed in a given chromosomal region as one variant can act as the surrogate for many others. Most recently, the association study design has been extended from the examination of a specific candidate gene to an unbiased, genome-wide approach.15 It has been estimated that in order to adequately survey the entire genome, a large number of genetic polymorphisms (250?000 to 1 million) is likely to be required.16�C18 However, the number of polymorphisms Smad inhibitor will vary between studies as different populations have different levels of LD. Genome-wide association studies (GWAS) utilize single nucleotide polymorphisms (SNP) as they are the most efficiently assayed type of genetic variant. In the most commonly used approach to GWAS the genotype frequencies at each SNP are compared between cases and controls. However, such a large number of comparisons requires the use of extremely stringent statistical correction to avoid an overwhelmingly large number of false positive results. For example, in a GWAS consisting of 500?000 SNP, to survive a Bonferroni correction requires a P-value?
