Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Athena Diagnostics | RCV000712879 | SCV000843430 | pathogenic | not provided | 2018-07-12 | criteria provided, single submitter | clinical testing | |
Human Genetics Bochum, |
RCV002463734 | SCV002758629 | likely pathogenic | Global developmental delay | 2022-02-17 | criteria provided, single submitter | clinical testing | ACMG criteria used to clasify this variant: PVS1, PM2_SUP |
Myriad Genetics, |
RCV003453516 | SCV004189686 | pathogenic | Cowden syndrome 1 | 2023-10-02 | criteria provided, single submitter | clinical testing | This variant is considered pathogenic. This variant creates a termination codon and is predicted to result in premature protein truncation. |
Ambry Genetics | RCV005260377 | SCV005927137 | pathogenic | Hereditary cancer-predisposing syndrome | 2025-02-12 | criteria provided, single submitter | clinical testing | The c.885_886delAT pathogenic mutation, located in coding exon 8 of the PTEN gene, results from a deletion of two nucleotides at nucleotide positions 885 to 886, causing a translational frameshift with a predicted alternate stop codon (p.C296*). This variant is considered to be rare based on population cohorts in the Genome Aggregation Database (gnomAD). 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. |