Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Laboratory for Molecular Medicine, |
RCV000037163 | SCV000060820 | pathogenic | Hypohidrotic X-linked ectodermal dysplasia | 2011-09-17 | criteria provided, single submitter | clinical testing | The Ser91fs variant in EDA has not been reported in the literature nor previousl y identified by our laboratory. This frameshift variant is predicted to alter t he protein?s amino acid sequence beginning at position 91 and lead to a prematur e termination codon 9 amino acids downstream. This alteration is then predicted to lead to a truncated or absent protein. Heterozygous loss of function of the E DA gene is an established disease mechanism in XLHED. In summary, this variant m eets our criteria to be classified as pathogenic (http://pcpgm.partners.org/LMM) . |
Labcorp Genetics |
RCV000037163 | SCV004330161 | pathogenic | Hypohidrotic X-linked ectodermal dysplasia | 2023-11-07 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Ser91Argfs*9) in the EDA gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in EDA are known to be pathogenic (PMID: 9683615). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with EDA-related conditions. ClinVar contains an entry for this variant (Variation ID: 44187). For these reasons, this variant has been classified as Pathogenic. |