We propose to consider a role for selected genes such as AATF (cell proliferation and apoptosis) and TADA2L (Wnt pathway) at the 17q12 region as well as developmental and transcriptional pathways represented by these genes, in the development of OA/TOF and VATER association.
The common ACE deletion polymorphism is associated with a greater than 2-fold increase in the odds of developing JET in children undergoing surgical repair of atrioventricular septal defect, Tetralogy of Fallot, ventricular septal defect or the Norwood and arterial switch procedures.
In our cohort, TOF was significantly associated with a genotyped single-nucleotide polymorphism (rs12519770, <i>P</i>=2.98×10<sup>-</sup><sup>8</sup>) in an intron of the adhesion <i>GPR98</i> (G-protein-coupled receptor V1) gene on chromosome 5q14.3.
Prenatal diagnosis and molecular cytogenetic characterization of a de novo 4.858-Mb microdeletion in 15q14 associated with ACTC1 and MEIS2 haploinsufficiency and tetralogy of Fallot.
In our cohort, TOF was significantly associated with a genotyped single-nucleotide polymorphism (rs12519770, <i>P</i>=2.98×10<sup>-</sup><sup>8</sup>) in an intron of the adhesion <i>GPR98</i> (G-protein-coupled receptor V1) gene on chromosome 5q14.3.
In our cohort, TOF was significantly associated with a genotyped single-nucleotide polymorphism (rs12519770, <i>P</i>=2.98×10<sup>-</sup><sup>8</sup>) in an intron of the adhesion <i>GPR98</i> (G-protein-coupled receptor V1) gene on chromosome 5q14.3.
The current study aimed to determine the effect of losartan, an angiotensin II receptor blocker, on subpulmonary RV dysfunction in adults after repaired tetralogy of Fallot.
In summary, our screen indicates that ALDH1A2 genetic variation is present in TOF patients, suggesting a possible causal role for this gene in rare cases of human CHD, but does not support the hypothesis that variation at the ALDH1A2 locus is a significant modifier of the risk for CHD in humans.
A prospective cohort of Tetralogy of Fallot (TOF) patients (n = 118) was recruited to investigate the influence of the ALDH2*2 allele on cardioprotection after surgical repair.
Infants with ventricular septal defect (VSD), tetralogy of Fallot (TOF), transposition of the great arteries (TGA), and hypoplastic left heart syndrome (HLHS) in a study of apolipoprotein E (APOE) polymorphisms, and neurodevelopmental outcome underwent neurodevelopmental and genetic evaluation at 4 years of age.
An aortic diameter of the ascending aorta, CAVI, and plasma TGF-β1 level were significantly higher in repaired TOF without ARB than those in controls, whereas baPWV did not differ.