Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Laboratory of Medical Genetics, |
RCV002287289 | SCV002577553 | pathogenic | Hereditary spherocytosis type 2 | 2022-01-24 | criteria provided, single submitter | clinical testing | PVS1, PM2, PP3, PP5 |
Gene |
RCV004812440 | SCV005437570 | pathogenic | not provided | 2024-06-10 | criteria provided, single submitter | clinical testing | Has been reported in a patient, who also harbored a variant in the SLC4A1 gene, with hereditary spherocytosis in published literature; familial segregation information and additional clinical information were not included in this report (PMID: 32436265); Nonsense variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 32436265) |
Labcorp Genetics |
RCV004812440 | SCV005782154 | pathogenic | not provided | 2024-07-20 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Trp1705*) in the SPTB gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SPTB are known to be pathogenic (PMID: 1391962, 1498324, 8844207, 26830532, 27292444). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with hereditary spherocytosis (PMID: 32436265). ClinVar contains an entry for this variant (Variation ID: 1708136). For these reasons, this variant has been classified as Pathogenic. |