Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001245306 | SCV001418584 | benign | Idiopathic generalized epilepsy; Hyperaldosteronism, familial, type IV | 2023-11-27 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001548338 | SCV001768232 | uncertain significance | not provided | 2021-03-05 | criteria provided, single submitter | clinical testing | In silico analysis supports that this missense variant does not alter protein structure/function; Has not been previously published as pathogenic or benign to our knowledge |
Fulgent Genetics, |
RCV002491825 | SCV002776672 | uncertain significance | Epilepsy, childhood absence, susceptibility to, 6; Hyperaldosteronism, familial, type IV | 2022-04-05 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV003365287 | SCV004064919 | uncertain significance | Inborn genetic diseases | 2023-07-17 | criteria provided, single submitter | clinical testing | The c.6817C>T (p.L2273F) alteration is located in exon 35 (coding exon 34) of the CACNA1H gene. This alteration results from a C to T substitution at nucleotide position 6817, causing the leucine (L) at amino acid position 2273 to be replaced by a phenylalanine (F). Based on insufficient or conflicting evidence, the clinical significance of this alteration remains unclear. |
Breakthrough Genomics, |
RCV001548338 | SCV005194087 | uncertain significance | not provided | criteria provided, single submitter | not provided |