Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV002378278 | SCV002667094 | pathogenic | Cardiovascular phenotype | 2016-03-08 | criteria provided, single submitter | clinical testing | The c.703delG pathogenic mutation, located in coding exon 5 of the ACVRL1 gene, results from a deletion of one nucleotide at nucleotide position 703, causing a translational frameshift with a predicted alternate stop codon (p.D235Mfs*23). Since frameshifts are typically deleterious in nature, this alteration is interpreted as a disease-causing mutation (ACMG Recommendations for Standards for Interpretation and Reporting of Sequence Variations. Revision 2007. Genet Med. 2008;10:294). |
Labcorp Genetics |
RCV003509729 | SCV004308033 | pathogenic | Telangiectasia, hereditary hemorrhagic, type 2 | 2023-05-30 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Asp235Metfs*23) 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). For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 1756828). This variant has not been reported in the literature in individuals affected with ACVRL1-related conditions. This variant is not present in population databases (gnomAD no frequency). |