Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000599086 | SCV000710097 | uncertain significance | not provided | 2020-10-30 | criteria provided, single submitter | clinical testing | Has not been previously published as pathogenic or benign to our knowledge; Reported in ClinVar (ClinVar Variant ID# 503802; Landrum et al., 2016); Not observed in large population cohorts (Lek et al., 2016); Nonsense variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss-of-function is not a well-established mechanism of disease for Loeys-Dietz syndrome, though nonsense variants in TGFBR1 have been reported in association with multiple self-healing squamous epithelioma (MSSE) in HGMD (Stenson et al., 2014) |
Labcorp Genetics |
RCV001058970 | SCV001223573 | pathogenic | Familial thoracic aortic aneurysm and aortic dissection | 2019-01-12 | criteria provided, single submitter | clinical testing | Loss-of-function variants in TGFBR1 are known to be pathogenic (PMID: 21358634). For these reasons, this variant has been classified as Pathogenic. This variant has not been reported in the literature in individuals with TGFBR1-related conditions. ClinVar contains an entry for this variant (Variation ID: 503802). This sequence change creates a premature translational stop signal (p.Tyr291*) in the TGFBR1 gene. It is expected to result in an absent or disrupted protein product. This variant is not present in population databases (ExAC no frequency). |