Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002000045 | SCV002229977 | pathogenic | Telangiectasia, hereditary hemorrhagic, type 2 | 2023-11-17 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Ser270Argfs*30) in the ACVRL1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ACVRL1 are known to be pathogenic (PMID: 15879500). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with hereditary hemorrhagic telangiectasia (Invitae). ClinVar contains an entry for this variant (Variation ID: 1452945). For these reasons, this variant has been classified as Pathogenic. |
Ambry Genetics | RCV002423133 | SCV002677056 | pathogenic | Cardiovascular phenotype | 2017-01-04 | criteria provided, single submitter | clinical testing | The c.807_810delGAGC pathogenic mutation, located in coding exon 6 of the ACVRL1 gene, results from a deletion of 4 nucleotides at nucleotide positions 807 to 810, causing a translational frameshift with a predicted alternate stop codon (p.S270Rfs*30). 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. |