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dc.contributor.authorDeardorff, Matthew A.
dc.contributor.authorSainz Maza, Jesús Vicente
dc.contributor.authorGrant, Struan F. A.
dc.contributor.otherUniversidad de Cantabriaes_ES
dc.date.accessioned2013-03-13T13:01:32Z
dc.date.available2013-03-13T13:01:32Z
dc.date.issued2011-02-03
dc.identifier.issn1741-7015
dc.identifier.urihttp://hdl.handle.net/10902/1843
dc.description.abstractThe hunt for the genetic contributors to complex disease has used a number of strategies, resulting in the identification of variants associated with many of the common diseases affecting society. However most of the genetic variants detected to date are single nucleotide polymorphisms (SNPs) and copy number variants (CNVs) and fall far short of explaining the full genetic component of any given disease. An as yet untapped genomic mechanism is somatic gene conversion and deletion, which could be complicit in disease risk but has been challenging to detect in genome-wide datasets. In a recent publication in BMC Medicine by Kenneth Ross, the author uses existing datasets to look at somatic gene conversion and deletion in human disease. Here, we describe how Ross's recent efforts to detect such occurrences could impact the field going forward.es_ES
dc.format.extent3 p.es_ES
dc.language.isoenges_ES
dc.publisherBioMed Centrales_ES
dc.rightsAtribución 3.0 Españaes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/
dc.sourceBMC Medicine. 2011 Feb 3;9:13es_ES
dc.titleAnother tool in the genome-wide association study arsenal: population-based detection of somatic gene conversiones_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsopenAccesses_ES
dc.identifier.DOI10.1186/1741-7015-9-13
dc.type.versionpublishedVersiones_ES


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Atribución 3.0 EspañaExcept where otherwise noted, this item's license is described as Atribución 3.0 España