Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute of Medical Genetics and Applied Genomics, |
RCV001682638 | SCV001905520 | pathogenic | not provided | 2021-09-15 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001682638 | SCV003805787 | pathogenic | not provided | 2023-02-17 | criteria provided, single submitter | clinical testing | Reported as an apparently de novo variant in a patient with facial dysmorphisms and delayed language and motor development in published literature, however, the full article was not available for review (Yan et al., 2020); Frameshift variant predicted to result in protein truncation, as the last 265 amino acids are replaced with 90 different amino acids, and other loss-of-function variants have been reported downstream in the Human Gene Mutation Database (HGMD); Not observed in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 32135595) |
3billion | RCV003314011 | SCV004013714 | pathogenic | Immunodeficiency 49 | criteria provided, single submitter | clinical testing | The variant is not observed in the gnomAD v2.1.1 dataset. The variant is predicted to result in a loss or disruption of normal protein function through protein truncation. The predicted truncated protein may be shortened by more than 10%. Similarly affected sibling shares the variant (3billion databse) The variant has been previously reported as de novo in a similarly affected individual (PMID: 32135595). The variant has been reported to be associated with BCL11B related disorder (ClinVar ID: VCV001275761 / PMID: 32135595). Therefore, this variant is classified as Pathogenic according to the recommendation of ACMG/AMP guideline. |