Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002526428 | SCV000550897 | likely pathogenic | Rienhoff syndrome | 2024-12-05 | criteria provided, single submitter | clinical testing | This sequence change replaces isoleucine, which is neutral and non-polar, with threonine, which is neutral and polar, at codon 322 of the TGFB3 protein (p.Ile322Thr). This variant is present in population databases (rs762643638, gnomAD 0.007%). This missense change has been observed in individuals with syndromic aortic aneurysms and dissections and/or TGFB3-related conditions (PMID: 25835445; internal data). It has also been observed to segregate with disease in related individuals. ClinVar contains an entry for this variant (Variation ID: 410276). Invitae Evidence Modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) indicates that this missense variant is expected to disrupt TGFB3 protein function with a positive predictive value of 80%. In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. |
Fulgent Genetics, |
RCV000763946 | SCV000894892 | uncertain significance | Arrhythmogenic right ventricular dysplasia 1; Rienhoff syndrome | 2018-10-31 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002374793 | SCV002690715 | uncertain significance | Familial thoracic aortic aneurysm and aortic dissection | 2020-06-16 | criteria provided, single submitter | clinical testing | The p.I322T variant (also known as c.965T>C), located in coding exon 6 of the TGFB3 gene, results from a T to C substitution at nucleotide position 965. The isoleucine at codon 322 is replaced by threonine, an amino acid with similar properties. This variant was reported in an individual from a thoracic aortic aneurysm and dissection (TAAD) cohort, and showed co-segregation with disease in his two children; however, clinical details were limited (Bertoli-Avella AM et al. J. Am. Coll. Cardiol., 2015 Apr;65:1324-1336). This amino acid position is highly conserved in available vertebrate species. In addition, this alteration is predicted to be deleterious by in silico analysis. Since supporting evidence is limited at this time, the clinical significance of this alteration remains unclear. |
Gene |
RCV003227758 | SCV003924965 | uncertain significance | not provided | 2022-11-15 | criteria provided, single submitter | clinical testing | Not observed at significant frequency in large population cohorts (gnomAD); In silico analysis supports that this missense variant has a deleterious effect on protein structure/function; This variant is associated with the following publications: (PMID: 29392890, 25835445) |