| Literature DB >> 21224895 |
Marie Cognet1, Agnés Nougayrede, Valérie Malan, Patrick Callier, Celia Cretolle, Laurence Faivre, David Genevieve, Alice Goldenberg, Delphine Heron, Sandra Mercier, Nicole Philip, Sabine Sigaudy, Alain Verloes, Sabine Sarnacki, Arnold Munnich, Michel Vekemans, Stanislas Lyonnet, Heather Etchevers, Jeanne Amiel, Loïc de Pontual.
Abstract
Feingold syndrome (FS) is a syndromic microcephaly entity for which MYCN is the major disease-causing gene. We studied the expression pattern of MYCN at different stages of human embryonic development and collected a series of 17 FS and 12 isolated oesophageal atresia (IOA) cases. An MYCN gene deletion/mutation was identified in 47% of FS cases exclusively. We hypothesized that mutations or deletions of highly conserved non-coding elements (HCNEs) at the MYCN locus could lead to its misregulation and thereby to FS and/or IOA. We subsequently sequenced five HCNEs at the MYCN locus and designed a high-density tiling path comparative genomic hybridization array of 3.3 Mb at the MYCN locus. We found no mutations or deletions in this region, supporting the hypothesis of genetic heterogeneity in FS.Entities:
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Year: 2011 PMID: 21224895 PMCID: PMC3083612 DOI: 10.1038/ejhg.2010.225
Source DB: PubMed Journal: Eur J Hum Genet ISSN: 1018-4813 Impact factor: 4.246