Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Genetic Services Laboratory, |
RCV001817790 | SCV002069206 | pathogenic | not provided | 2018-06-18 | criteria provided, single submitter | clinical testing | DNA sequence analysis of the ATP7B gene demonstrated the c.2605G>T sequence change in exon 11, that results in the creation of a premature stop codon at amino acid position 869, p.Gly869*. This pathogenic sequence change is predicted to result in an abnormal transcript, which may be degraded, or may lead to the production of a truncated ATP7B protein with potentially abnormal function. Truncating variants in ATP7B have been previously described in patients with Wilson disease (PMID: 18373411). This sequence change was identified with another pathogenic ATP7B variant in a patient. |
Labcorp Genetics |
RCV002542703 | SCV002950507 | pathogenic | Wilson disease | 2023-08-01 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 1338419). This premature translational stop signal has been observed in individual(s) with Wilson disease (PMID: 31708252). This variant is present in population databases (rs191312027, gnomAD 0.0009%). This sequence change creates a premature translational stop signal (p.Gly869*) in the ATP7B gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ATP7B are known to be pathogenic (PMID: 10441329, 16283883). |
Baylor Genetics | RCV002542703 | SCV004210685 | pathogenic | Wilson disease | 2022-03-02 | criteria provided, single submitter | clinical testing |