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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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Measuring outcomes in craniofacial and pediatric plastic surgery.

TL;DR: The challenges in measuring the standard outcomes of function, aesthetics, and health-related quality of life are discussed, along with the importance of developing evidence and studying quality improvement in this specialty.
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Cellular and developmental basis of orofacial clefts.

TL;DR: The latest cellular and developmental findings may provide a basis for better understanding of the underlying genetic, epigenetic, environmental, and molecular mechanisms of OFCs.
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Evaluation of exposure to contaminated drinking water and specific birth defects and childhood cancers at Marine Corps Base Camp Lejeune, North Carolina: a case–control study

TL;DR: A case control study to determine if children born during 1968–1985 to mothers with residential exposure to contaminated drinking water at Camp Lejeune during pregnancy were more likely to have childhood hematopoietic cancers, neural tube defects (NTDs), or oral clefts.
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Non-syndromic cleft lip and/or cleft palate: Epidemiology and risk factors in Lubumbashi (DR Congo), a case-control study.

TL;DR: Several environmental risk factors highly prevalent in Central Africa for facial clefting were found and significant associations with a family history of cleft lip and palate were found.
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Identification of shared and unique gene families associated with oral clefts

TL;DR: The results indicate inherent differences in the genetic etiologies that underlie oral cleft phenotypes and support epidemiological evidence that genes associated with CL/P are both developmentally and genetically different from CP only, incomplete CP, and submucous CP.
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