COMMENTARY

Crohn's disease

The promise and perils of interpreting genetic associations in Crohn’s disease

T T Trinh¹, J D Rioux²

¹ The Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA, and University of Virginia Health System, Digestive Health Center of Excellence, Charlottesville, Virginia, USA
² The Broad Institute of MIT and Harvard, Brigham and Women’s Hospital, Department of Neurology, Harvard Medical School, Cambridge, Massachusetts, USA, and Université de Montréal, Montreal Heart Institute, Montréal, Québec, Canada

Correspondence to:
Correspondence to:
Dr John D Rioux
5000 Rue Bélanger, Montréal, Québec, Canada; rioux@broad.mit.edu

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Extended analyses of inflammatory bowel disease susceptibility loci is advisable before definitive conclusions about their causative role can be drawn

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Keywords: Crohn’s disease; phenotypes; polymorphisms; IBD5; DLG5; OCTNs

The first 150 words of the full text of this article appear below.

Genome wide linkage analysis has been an extremely successful method for mapping rare but highly penetrant genes in monogenic disorders.¹ Its applications to common diseases have achieved limited success, however, due to the individually low heritability of each contributing gene.² Alternatively, association based genetic studies, as described by Risch and Merikangas,³ can be powerful tools for identifying causal genes in common human diseases.^1,4 To date, these methods have been used to follow up on linkage regions and to test for candidate genes and therefore have been limited by the previous linkage analyses or by the assumptions made regarding disease pathogenesis. Both of these factors can greatly diminish our ability to detect all possible causal variants contributing to complex disease traits. Over the last decade, however, technology and genetic resources have evolved dramatically. With the completion of the human genome sequence, recent development of high throughput genotyping technologies and . . . [Full text of this article]

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