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Cleft lip and palate

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TLDR
Prevention is the ultimate objective for clefts of the lip and palate, and a prerequisite of this aim is to elucidate causes of the disorders.
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This article is published in The Lancet.The article was published on 2009-11-21. It has received 1344 citations till now. The article focuses on the topics: Oral cleft & IRF6.

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Citations
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Association between NOGGIN and SPRY2 polymorphisms and nonsyndromic cleft lip with or without cleft palate.

TL;DR: Investigation of association of SNPs of noggin (NOG) and sprouty homolog 2 (SPRY2) with NSCLP risk found NOG rs227731 genotype was associated with decreased NSCLp risk in a Northern Chinese population.
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Network-based identification of critical regulators as putative drivers of human cleft lip

TL;DR: This work presents a global view of the CL regulatory network and a novel approach on investigating critical miRNAs, TFs and genes via combinatory regulatory networks in craniofacial development.
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The Role of the Wnt Signaling Pathway in Upper Jaw Development of Chick Embryo.

TL;DR: The data suggest that the Wnt signaling pathway regulates maxillary morphogenesis and growth through Bmp4, Tbx22, Sox9, and Barx1 and might regulate N-cadherin expression via Msx1, resulting in cell aggregation for osteochondrogenesis.
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TBX22 mutation associated with cleft lip/palate, hypodontia, and limb anomaly.

TL;DR: It is demonstrated that TBX22 mutation is associated not only with cleft palate and ankyloglossia, but also cleft lip and palate and tooth agenesis, and Phenotypic variability caused by a single nucleotide substitution is clearly demonstrated.
References
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Journal ArticleDOI

Retinoic Acid Embryopathy

TL;DR: It is possible that a major mechanism of isotretinoin teratogenesis is a deleterious effect on cephalic neural-crest cell activity that results in the observed craniofacial, cardiac, and thymic malformations.
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Apaf1 (CED-4 homolog) regulates programmed cell death in mammalian development.

TL;DR: It is suggested that Apaf1 is essential for Casp3 activation in embryonic brain and is a key regulator of developmental programmed cell death in mammals.
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Clinical manifestations in 105 persons with nevoid basal cell carcinoma syndrome.

TL;DR: The frequency of the clinical and radiological anomalies in Nevoid basal cell carcinoma syndrome in a large population of US patients is delineated and guidelines for diagnosis and management are discussed.
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Transforming growth factor-β3 is required for secondary palate fusion

TL;DR: This result demonstrates that TGF–β3 affects palatal shelf fusion by an intrinsic, primary mechanism rather than by effects secondary to craniofacial defects.
Related Papers (5)

A genome-wide association study of cleft lip with and without cleft palate identifies risk variants near MAFB and ABCA4