Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Prevention |
RCV000679597 | SCV000806712 | uncertain significance | not provided | 2017-01-06 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV001010161 | SCV001170316 | uncertain significance | Hereditary cancer-predisposing syndrome | 2018-12-29 | criteria provided, single submitter | clinical testing | The p.Q394* variant (also known as c.1180C>T), located in coding exon 12 of the POLE gene, results from a C to T substitution at nucleotide position 1180. This changes the amino acid from a glutamine to a stop codon within coding exon 12. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. However, loss of function via haploinsufficiency in POLE has not been clearly established as a mechanism of disease. Since supporting evidence is limited at this time, the clinical significance of this alteration remains unclear. |
Labcorp Genetics |
RCV000679597 | SCV002197715 | pathogenic | not provided | 2024-08-05 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln394*) in the POLE gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in POLE are known to be pathogenic (PMID: 23230001, 25948378, 30503519). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with POLE-related conditions. ClinVar contains an entry for this variant (Variation ID: 560839). For these reasons, this variant has been classified as Pathogenic. |