Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000400090 | SCV000333775 | pathogenic | not provided | 2015-09-14 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV002487195 | SCV002787855 | likely pathogenic | COACH syndrome 1; Joubert syndrome 6; Meckel syndrome, type 3; RHYNS syndrome; Bardet-Biedl syndrome 14; Nephronophthisis 11 | 2024-03-29 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV002518850 | SCV003512559 | pathogenic | Familial aplasia of the vermis; Meckel-Gruber syndrome | 2024-11-03 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Ser288*) in the TMEM67 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in TMEM67 are known to be pathogenic (PMID: 20232449, 23559409). This variant is present in population databases (rs769957689, gnomAD 0.01%). This variant has not been reported in the literature in individuals affected with TMEM67-related conditions. ClinVar contains an entry for this variant (Variation ID: 282355). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV000400090 | SCV003924744 | likely pathogenic | not provided | 2023-05-14 | criteria provided, single submitter | clinical testing | Nonsense 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; Not observed at significant frequency in large population cohorts (gnomAD); Has not been previously published as pathogenic or benign to our knowledge; This variant is associated with the following publications: (PMID: 31589614) |