Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001069053 | SCV001234197 | pathogenic | not provided | 2023-06-23 | criteria provided, single submitter | clinical testing | This variant is present in population databases (rs746419489, gnomAD 0.002%). This sequence change creates a premature translational stop signal (p.Tyr39*) in the HOGA1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in HOGA1 are known to be pathogenic (PMID: 22391140, 22781098). This premature translational stop signal has been observed in individual(s) with primary hyperoxaluria (PMID: 22391140). ClinVar contains an entry for this variant (Variation ID: 204268). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site. For these reasons, this variant has been classified as Pathogenic. |
Clinical Biochemistry Laboratory, |
RCV000186475 | SCV000239834 | pathogenic | Primary hyperoxaluria type 3 | 2014-11-27 | no assertion criteria provided | research | |
Natera, |
RCV000186475 | SCV002094504 | pathogenic | Primary hyperoxaluria type 3 | 2020-12-24 | no assertion criteria provided | clinical testing |