Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Clin |
RCV000851671 | SCV005061686 | likely pathogenic | Glanzmann thrombasthenia | 2024-05-02 | reviewed by expert panel | curation | The NM_000419.5(ITGA2B):c.1211-1G>C splice variant is predicted to result in the loss of exon 13, causing an in-frame deletion of 60 amino acids. This exon loss occurs within the critical ligand binding extracellular domain (PVS1_strong). The variant is absent from gnomADv4.0.0 (PM2_supporting). The variant has has been reported in one homozygous patient stated to Glanzmann thrombasthenia (PM3_supporting, PMID: 31064749). In summary, this variant meets the criteria to be classified as Likely Pathogenic for autosomal recessive Glanzmann Thrombasthenia based on the ACMG/AMP criteria applied, as specified by the ClinGen PD VCEP: PM2_Supporting, PM3_supporting, PVS1_strong (PD VCEP specifications version 2.1). |
NIHR Bioresource Rare Diseases, |
RCV000851671 | SCV000899455 | likely pathogenic | Glanzmann thrombasthenia | 2019-02-01 | criteria provided, single submitter | research |