Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000662864 | SCV000785749 | uncertain significance | Colorectal cancer, susceptibility to, 12 | 2017-11-27 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003656650 | SCV001516808 | pathogenic | not provided | 2024-09-01 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Asp1211*) 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: 548812). For these reasons, this variant has been classified as Pathogenic. |
Ambry Genetics | RCV002458177 | SCV002615944 | uncertain significance | Hereditary cancer-predisposing syndrome | 2020-05-04 | criteria provided, single submitter | clinical testing | The c.3629dupC variant, located in coding exon 30 of the POLE gene, results from a duplication of C at nucleotide position 3629, causing a translational frameshift with a predicted alternate stop codon (p.D1211*). This alteration is expected to result in premature protein truncation or nonsense-mediated mRNA decay. However, loss of function of 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. |