Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ce |
RCV001091003 | SCV001246826 | likely pathogenic | not provided | 2019-10-01 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001368415 | SCV001564810 | pathogenic | Tumor predisposition syndrome 3 | 2021-08-17 | criteria provided, single submitter | clinical testing | This variant is not present in population databases (ExAC no frequency). This variant has not been reported in the literature in individuals affected with POT1-related conditions. ClinVar contains an entry for this variant (Variation ID: 871194). For these reasons, this variant has been classified as Pathogenic. This sequence change creates a premature translational stop signal (p.Ala356Serfs*15) in the POT1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in POT1 are known to be pathogenic (PMID: 32155570). |
Ambry Genetics | RCV002411626 | SCV002723392 | pathogenic | Hereditary cancer-predisposing syndrome | 2021-08-13 | criteria provided, single submitter | clinical testing | The c.1065dupA pathogenic mutation, located in coding exon 9 of the POT1 gene, results from a duplication of A at nucleotide position 1065, causing a translational frameshift with a predicted alternate stop codon (p.A356Sfs*15). 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. |