Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000665849 | SCV000790035 | likely pathogenic | Ellis-van Creveld syndrome | 2017-03-02 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001045278 | SCV001209118 | pathogenic | Ellis-van Creveld syndrome; Curry-Hall syndrome | 2023-12-21 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Tyr121*) in the EVC gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in EVC are known to be pathogenic (PMID: 23220543). This variant is present in population databases (no rsID available, gnomAD 0.003%). This premature translational stop signal has been observed in individual(s) with Ellis–van Creveld syndrome or short-rib polydactyly syndrome type II (PMID: 19810119, 29068549). ClinVar contains an entry for this variant (Variation ID: 446662). For these reasons, this variant has been classified as Pathogenic. |
Dan Cohn Lab, |
RCV000516149 | SCV000612082 | pathogenic | Short-rib thoracic dysplasia 6 with or without polydactyly | 2017-06-01 | no assertion criteria provided | research | |
University of Washington Center for Mendelian Genomics, |
RCV000516149 | SCV001479597 | likely pathogenic | Short-rib thoracic dysplasia 6 with or without polydactyly | no assertion criteria provided | research | ||
Natera, |
RCV000665849 | SCV002083013 | pathogenic | Ellis-van Creveld syndrome | 2020-11-09 | no assertion criteria provided | clinical testing |