Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV002357983 | SCV002655097 | pathogenic | Hereditary cancer-predisposing syndrome | 2019-09-10 | criteria provided, single submitter | clinical testing | The c.5dupC pathogenic mutation, located in coding exon 1 of the SDHA gene, results from a duplication of C at nucleotide position 5, causing a translational frameshift with a predicted alternate stop codon (p.V4Gfs*35). 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. |
Labcorp Genetics |
RCV003098098 | SCV003452679 | pathogenic | Mitochondrial complex II deficiency, nuclear type 1; Paragangliomas 5 | 2024-01-17 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Val4Glyfs*35) in the SDHA gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SDHA are known to be pathogenic (PMID: 22974104, 24781757). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with SDHA-related conditions. ClinVar contains an entry for this variant (Variation ID: 1750996). For these reasons, this variant has been classified as Pathogenic. |
Myriad Genetics, |
RCV004052556 | SCV004930718 | pathogenic | Paragangliomas 5 | 2024-02-06 | criteria provided, single submitter | clinical testing | This variant is considered pathogenic. This variant creates a frameshift predicted to result in premature protein truncation. |