Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002046716 | SCV002108393 | pathogenic | Tumor predisposition syndrome 3 | 2022-09-19 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. ClinVar contains an entry for this variant (Variation ID: 1348991). This variant has not been reported in the literature in individuals affected with POT1-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.His211Profs*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 | RCV002359284 | SCV002655224 | pathogenic | Hereditary cancer-predisposing syndrome | 2021-03-24 | criteria provided, single submitter | clinical testing | The c.631dupC pathogenic mutation, located in coding exon 5 of the POT1 gene, results from a duplication of C at nucleotide position 631, causing a translational frameshift with a predicted alternate stop codon (p.H211Pfs*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. |