Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000557187 | SCV000632084 | likely benign | Idiopathic generalized epilepsy; Hyperaldosteronism, familial, type IV | 2024-12-07 | criteria provided, single submitter | clinical testing | |
Center for Genomics, |
RCV003224322 | SCV003919755 | uncertain significance | Epilepsy, childhood absence, susceptibility to, 6; Hyperaldosteronism, familial, type IV | 2021-03-30 | criteria provided, single submitter | clinical testing | CACNA1H NM_021098.2 exon 9 p.Arg503His (c.1508G>A): This variant has not been reported in the literature but is present in 0.1% (16/15288) of African alleles in the Genome Aggregation Database (https://gnomad.broadinstitute.org/variant/16-1251958-G-A). This variant is present in ClinVar (Variation ID:460048). Evolutionary conservation and computational predictive tools for this variant are unclear. In summary, data on this variant is insufficient for disease classification. Therefore, the clinical significance of this variant is uncertain. |
Ambry Genetics | RCV004023824 | SCV004915116 | uncertain significance | Inborn genetic diseases | 2021-07-15 | criteria provided, single submitter | clinical testing | The c.1508G>A (p.R503H) alteration is located in exon 9 (coding exon 8) of the CACNA1H gene. This alteration results from a G to A substitution at nucleotide position 1508, causing the arginine (R) at amino acid position 503 to be replaced by a histidine (H). Based on insufficient or conflicting evidence, the clinical significance of this alteration remains unclear. |
Gene |
RCV004719856 | SCV005325888 | uncertain significance | not provided | 2024-02-08 | criteria provided, single submitter | clinical testing | In silico analysis supports that this missense variant does not alter protein structure/function; This variant is associated with the following publications: (PMID: 35668055) |