Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Clin |
RCV000851591 | SCV001397538 | pathogenic | Glanzmann thrombasthenia | 2020-09-06 | reviewed by expert panel | curation | The nonsense variant, NM_000419.4:c.2344C>T (p.Arg782Ter) is expected to cause NMD of the resulting transcript. The variant is absent from population databases. The variant is reported in one compound heterozygous individual with the frameshift variant, Leu973AlafsTer63 (PMID: 28888044) and two homozygous individuals in (PMID: 31064749). In summary, based on the evidence available at this time, the variant is classified as pathogenic. GT-specific criteria applied: PVS1, PP4_moderate, PM2_supporting, PM3_supporting. |
NIHR Bioresource Rare Diseases, |
RCV000851591 | SCV000899324 | likely pathogenic | Glanzmann thrombasthenia | 2019-02-01 | criteria provided, single submitter | research | |
Labcorp Genetics |
RCV000851591 | SCV004298232 | pathogenic | Glanzmann thrombasthenia | 2023-04-11 | 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: 626927). This premature translational stop signal has been observed in individual(s) with clinical features of Glanzmann thrombasthenia (PMID: 28888044, 31064749). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Arg782*) in the ITGA2B gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ITGA2B are known to be pathogenic (PMID: 21917754). |