Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV001266179 | SCV001444351 | pathogenic | Inborn genetic diseases | 2021-01-15 | criteria provided, single submitter | clinical testing | The c.325dupC (p.Q109Pfs*3) alteration, located in exon 3 (coding exon 1) of the NR4A2 gene, consists of a duplication of C at position 325, causing a translational frameshift with a predicted alternate stop codon after 3 amino acids. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. Based on data from the Genome Aggregation Database (gnomAD) database, the NR4A2 c.325dupC alteration was observed in 0.0004% (1/250,966) of total alleles studied. Based on the available evidence, this alteration is classified as pathogenic. |
Institute of Human Genetics, |
RCV001724280 | SCV001950012 | pathogenic | Neurodevelopmental disorder | 2021-11-23 | criteria provided, single submitter | clinical testing | This variant was identified as de novo (maternity and paternity confirmed)._x000D_ Criteria applied: PVS1, PS2, PS4_SUP, PM2_SUP |
Gene |
RCV002275338 | SCV002562512 | pathogenic | not provided | 2023-11-12 | criteria provided, single submitter | clinical testing | Frameshift 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; This variant is associated with the following publications: (PMID: 32366965) |
OMIM | RCV002260695 | SCV002540594 | pathogenic | Intellectual developmental disorder with language impairment and early-onset DOPA-responsive dystonia-parkinsonism | 2022-06-22 | no assertion criteria provided | literature only |