Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001063612 | SCV001228467 | pathogenic | Telangiectasia, hereditary hemorrhagic, type 2 | 2019-01-27 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Trp399*) in the ACVRL1 gene. It is expected to result in an absent or disrupted protein product. This variant is not present in population databases (ExAC no frequency). For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in ACVRL1 are known to be pathogenic (PMID: 15879500). A different variant (c.1197G>A) giving rise to the same protein effect observed here (p.Trp399*) has been determined to be pathogenic (Invitae). This suggests that this variant is also likely to be causative of disease. This variant has not been reported in the literature in individuals with ACVRL1-related conditions. |
Ambry Genetics | RCV002339315 | SCV002640588 | pathogenic | Cardiovascular phenotype | 2018-12-29 | criteria provided, single submitter | clinical testing | The p.W399* pathogenic mutation (also known as c.1196G>A), located in coding exon 7 of the ACVRL1 gene, results from a G to A substitution at nucleotide position 1196. This changes the amino acid from a tryptophan to a stop codon within coding exon 7. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |