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Sabata C. Lund

Researcher at University of Michigan

Publications -  7
Citations -  4576

Sabata C. Lund is an academic researcher from University of Michigan. The author has contributed to research in topics: Autism & Genome-wide association study. The author has an hindex of 7, co-authored 7 publications receiving 4224 citations. Previous affiliations of Sabata C. Lund include Vanderbilt University & Stanford University.

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Journal ArticleDOI

Functional impact of global rare copy number variation in autism spectrum disorders

Dalila Pinto, +181 more
- 15 Jul 2010 - 
TL;DR: The genome-wide characteristics of rare (<1% frequency) copy number variation in ASD are analysed using dense genotyping arrays to reveal many new genetic and functional targets in ASD that may lead to final connected pathways.
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Multiple Recurrent De Novo CNVs, Including Duplications of the 7q11.23 Williams Syndrome Region, Are Strongly Associated with Autism

Stephen Sanders, +66 more
- 09 Jun 2011 - 
TL;DR: A genome-wide analysis of rare copy-number variation in 1124 autism spectrum disorder families, each comprised of a single proband, unaffected parents, and, in most kindreds, an unaffected sibling, finds significant association of ASD with de novo duplications of 7q11.23, where the reciprocal deletion causes Williams-Beuren syndrome.
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A genome-wide scan for common alleles affecting risk for autism

Richard Anney, +170 more
TL;DR: In one of four primary association analyses, the association signal for marker rs4141463, located within MACROD2, crossed the genome-wide association significance threshold of P < 5 × 10−8 and, consistent with the winner's curse, its effect size in the replication sample was much smaller.
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Individual common variants exert weak effects on the risk for autism spectrum disorders.

Richard Anney, +148 more
TL;DR: Stage 2 of the Autism Genome Project genome-wide association study is reported, adding 1301 ASD families and bringing the total to 2705 families analysed, and it is reasonable to conclude that common variants affect the risk for ASD but their individual effects are modest.