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.About:
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.read more
Citations
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A systematic review of associated structural and chromosomal defects in oral clefts: when is prenatal genetic analysis indicated?
Wies Maarse,Anna M. Rozendaal,Anna M. Rozendaal,Eva Pajkrt,Christl Vermeij-Keers,Aebele B. Mink van der Molen,Marie-José H. van den Boogaard +6 more
TL;DR: Prenatal counselling regarding prognosis and risk of chromosomal defects should be tailored to cleft category, and more importantly to the presence/absence of associated anomalies.
Journal ArticleDOI
Parental age as a risk factor for non-syndromic oral clefts: a meta-analysis.
Ana Paula Corrêa de Queiroz Herkrath,Fernando José Herkrath,Maria Augusta Bessa Rebelo,Mario Vianna Vettore +3 more
TL;DR: It is suggested that fathers forty years of age or older had a 58% higher probability of having a child with cleft palate compared to those aged between 20 and 39 years, and no evidence of association between early maternal and paternal age with occurrence of oral clefts was observed.
Journal ArticleDOI
Expression and mutation analyses implicate ARHGAP29 as the etiologic gene for the cleft lip with or without cleft palate locus identified by genome-wide association on chromosome 1p22.
Elizabeth J. Leslie,M. Adela Mansilla,Leah C. Biggs,Kristi Schuette,Steve Bullard,Margaret E. Cooper,Martine Dunnwald,Andrew C. Lidral,Mary L. Marazita,Terri H. Beaty,Jeffrey C. Murray +10 more
TL;DR: A novel pathway in which the IRF6 gene regulatory network interacts with the Rho pathway via ARHGAP29 is suggested, which is suggested to be the etiologic gene at the 1p22 genome-wide association study locus for NSCL/P.
Journal ArticleDOI
Cleft Lip and Palate.
TL;DR: After definitive repair, children remain at increased risk for middle ear disease, velopharyngeal dysfunction, and malocclusion and require ongoing follow-up with a multidisciplinary team.
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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Women and smoking: a report of the Surgeon General.
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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.
Virginia Kimonis,Alisa M. Goldstein,B. Pastakia,Mu Yang,Ronald G. Kase,John J. DiGiovanna,Allen E. Bale,Sherri J. Bale +7 more
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.
Journal ArticleDOI
Transforming growth factor-β3 is required for secondary palate fusion
Gabriele Proetzel,Sharon A. Pawlowski,Michael V. Wiles,Moying Yin,Gregory P. Boivin,Philip N. Howles,Jixang Ding,Mark W. J. Ferguson,Thomas Doetschman +8 more
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.
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