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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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Dexamethasone Induces Apoptosis of Embryonic Palatal Mesenchymal Cells Through the GATA-6/Bone Morphogenetic Protein-2/p38 MAPK Pathway

TL;DR: In this paper , the authors investigated the mechanism of DEX-induced cleft palate formation and showed that GATA binding protein 6 (GATA-6)/bone morphogenetic protein-2 (BMP-2) mediated apoptosis.
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Significance of E-cadherin Gene Mutations in Patients With Hereditary Diffuse Gastric Cancer Syndrome: A Systematic Review.

TL;DR: A total of 10 studies on review with different study populations showed that of the 42 patients who were diagnosed with diffuse gastric cancer, 88% of them showed a positive germline E-cadherin gene mutation and 100% of the CDH1 mutation carriers showed microscopic changes of signet ring cell adenocarcinoma of the stomach.
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Seasonal Influence on the Numbers of Gender-Related Orofacial Cleft Conceptions in the Netherlands.

TL;DR: In the multifactorial etiology of orofacial clefts (OFCs), environmental factors play an important role as mentioned in this paper, and to trace the influence of these factors, the timing of the cell biological mechan...
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Characteristics of craniofacial morphology and factors affecting them in patients with isolated cleft palate.

TL;DR: In this paper, the characteristics of cranio-facial morphology in patients with isolated cleft palate (ICP) and investigate the clinical factors affecting these categorised morphological characteristics.
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