Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Devlin, B. et al.

No evidence for linkage of liability to autism to HOXA1 in a sample from the CPEA network.

A recent study by Ingram et al. [2000b: Teratology 62:393-405] suggests a (His)73(Arg) polymorphism (A:G) in HOXA1 contributes substantially to a liability for autism. Using 68 individuals diagnosed with Autism Spectrum Disorders, they found a significant dearth of G homozygotes and biased transmission of G alleles from parents to affected offspring, especially from mothers. Because the connection between HOXA1 and liability to autism is compelling, we attempted to replicate their finding using a larger, independent sample from the Collaborative Programs of Excellence in Autism (CPEA) network. In our data, genotype frequencies conform to Hardy-Weinberg equilibrium; allele transmissions meet Mendelian expectations; and there is no obvious sex-biased allele transmission. Based on our sample size, calculations suggest that we would have at least 95% power to detect linkage and association even if the A:G polymorphism were to account for only 1% of the heritability of autism. Therefore, although we cannot exclude the possibility that the samples in the two studies are intrinsically different, our data from our sample argue against a major role for HOXA1 (His)73(Arg) in liability to autism.[1]

References

No evidence for linkage of liability to autism to HOXA1 in a sample from the CPEA network. Devlin, B., Bennett, P., Cook, E.H., Dawson, G., Gonen, D., Grigorenko, E.L., McMahon, W., Pauls, D., Smith, M., Spence, M.A., Schellenberg, G.D. Am. J. Med. Genet. (2002) [Pubmed]

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