| Literature DB >> 26123647 |
Luciano Abreu Brito1, Guilherme Lopes Yamamoto1, Soraia Melo2,3, Carolina Malcher1, Simone Gomes Ferreira1, Joana Figueiredo2,3, Lucas Alvizi1, Gerson Shigeru Kobayashi1, Michel Satya Naslavsky1, Nivaldo Alonso4, Temis Maria Felix5, Mayana Zatz1, Raquel Seruca2,3,6, Maria Rita Passos-Bueno1.
Abstract
Nonsyndromic orofacial cleft (NSOFC) is a complex disease of still unclear genetic etiology. To investigate the contribution of rare epithelial cadherin (CDH1) gene variants to NSOFC, we target sequenced 221 probands. Candidate variants were evaluated via in vitro, in silico, or segregation analyses. Three probably pathogenic variants (c.760G>A [p.Asp254Asn], c.1023T>G [p.Tyr341*], and c.2351G>A [p.Arg784His]) segregated according to autosomal dominant inheritance in four nonsyndromic cleft lip with or without cleft palate (NSCL/P) families (Lod score: 5.8 at θ = 0; 47% penetrance). A fourth possibly pathogenic variant (c.387+5G>A) was also found, but further functional analyses are needed (overall prevalence of CDH1 candidate variants: 2%; 15.4% among familial cases). CDH1 mutational burden was higher among probands from familial cases when compared to that of controls (P = 0.002). We concluded that CDH1 contributes to NSCL/P with mainly rare, moderately penetrant variants, and CDH1 haploinsufficiency is the likely etiological mechanism.Entities:
Keywords: CDH1; gastric cancer; oral clefts; rare variant; two-hit model
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Year: 2015 PMID: 26123647 DOI: 10.1002/humu.22827
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878