Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000670205 | SCV000795035 | likely pathogenic | Ellis-van Creveld syndrome | 2017-10-25 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000702796 | SCV000831666 | pathogenic | Ellis-van Creveld syndrome; Curry-Hall syndrome | 2024-01-26 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg874*) in the EVC2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in EVC2 are known to be pathogenic (PMID: 17024374, 19810119, 19876929). This variant is present in population databases (rs760382778, gnomAD 0.003%). This premature translational stop signal has been observed in individual(s) with Ellis van Creveld (EvC) syndrome (PMID: 19251731). ClinVar contains an entry for this variant (Variation ID: 554547). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV001560317 | SCV001782703 | likely pathogenic | not provided | 2021-03-08 | criteria provided, single submitter | clinical testing | Has been reported previously in an individual with Ellis-van Creveld syndrome who also harbored a missense variant (Sund et al., 2009); 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 a significant frequency in large population cohorts (Lek et al., 2016); This variant is associated with the following publications: (PMID: 31589614, 25525159, 19251731) |