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Journal ArticleDOI

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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A functional polymorphism in the pre-miR-146a gene is associated with the risk of nonsyndromic orofacial cleft.

TL;DR: It is demonstrated that miR‐146a/rs2910164 is associated with susceptibility to NSOC, providing novel insights into the genetic etiology and underlying biology of NSOC.
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Developing palatal bone using human mesenchymal stem cell and stem cells from exfoliated deciduous teeth cell sheets.

TL;DR: It is shown that osteogenic stem cell sheets have mineralization potential and might represent a new alternative to autologous bone transplantation in the reconstruction of cleft palates.
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Gene expression profiling analysis contributes to understanding the association between non-syndromic cleft lip and palate, and cancer

TL;DR: The TP53, CDK1, SMAD3, PIK3R1 and CASP3 genes were found to be associated, not only with NSCL/P, but also with cancer.
Journal ArticleDOI

BHMT gene polymorphisms as risk factors for cleft lip and cleft palate in a Chinese population

TL;DR: It is suggested that polymorphism rs3797546 in the BHMT gene may confer genetic risk of NSCL/P in a recessive manner.
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Variations in WNT3 gene are associated with incidence of non-syndromic cleft lip with or without cleft palate in a northeast Chinese population.

TL;DR: The association between the WNT3 variant and NSCL/P in the population tested was confirmed and the P values for the haplotype of rs3809857-rs9890413 were observed to be statistically significant.
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.
Journal ArticleDOI

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