Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000665782 | SCV000789954 | likely pathogenic | Ellis-van Creveld syndrome | 2017-02-28 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001202364 | SCV001373474 | likely pathogenic | Ellis-van Creveld syndrome; Curry-Hall syndrome | 2024-01-04 | criteria provided, single submitter | clinical testing | This variant results in the deletion of part of exon 14 (c.1887-5_1904del) of the EVC gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in EVC are known to be pathogenic (PMID: 23220543). This variant is present in population databases (rs779275317, gnomAD 0.05%). This variant has been observed in individual(s) with Ellis-van Creveld syndrome (PMID: 19251731). This variant is also known as Del IVS13 (-9 to +14). ClinVar contains an entry for this variant (Variation ID: 550897). In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. |
Gene |
RCV001584533 | SCV001812810 | pathogenic | not provided | 2023-04-04 | criteria provided, single submitter | clinical testing | Deletion predicted to destroy the canonical splice acceptor site in a gene for which loss-of-function is a known mechanism of disease; Reported as likely pathogenic in ClinVar but additional evidence is not available (ClinVar Variation ID 550897; ClinVar); This variant is associated with the following publications: (PMID: 26582918, 19251731) |
Prevention |
RCV003403539 | SCV004104112 | pathogenic | EVC-related disorder | 2022-12-19 | criteria provided, single submitter | clinical testing | The EVC c.1887-5_1904del23 variant is predicted to result in a deletion affecting a canonical splice site. This variant was reported to be pathogenic for Ellis-van Creveld syndrome (see example: Figure 2A, Aubert-Mucca et al. 2022. PubMed ID: 35927022). This variant is reported in 0.046% of alleles in individuals of African descent in gnomAD (http://gnomad.broadinstitute.org/variant/4-5798739-TTCCTCAAAGGTCCACGCGGTGTG-T). This variant is interpreted as pathogenic. |