Total submissions: 5
| Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
|---|---|---|---|---|---|---|---|---|
| Revvity Omics, |
RCV001780601 | SCV002018097 | pathogenic | Deficiency of steroid 17-alpha-monooxygenase | 2019-05-01 | criteria provided, single submitter | clinical testing | |
| Labcorp Genetics |
RCV001885149 | SCV002237753 | pathogenic | not provided | 2024-07-24 | criteria provided, single submitter | clinical testing | This sequence change replaces proline, which is neutral and non-polar, with arginine, which is basic and polar, at codon 409 of the CYP17A1 protein (p.Pro409Arg). This variant is present in population databases (rs367833709, gnomAD 0.03%). This missense change has been observed in individual(s) with 17-alpha-hydroxylase deficiency (PMID: 11243732, 20170344, 22087567, 22954317). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. This variant is also known as g.5582C>G. ClinVar contains an entry for this variant (Variation ID: 1322182). An algorithm developed to predict the effect of missense changes on protein structure and function (PolyPhen-2) suggests that this variant is likely to be disruptive. Experimental studies have shown that this missense change affects CYP17A1 function (PMID: 11243732, 23291414). For these reasons, this variant has been classified as Pathogenic. |
| Fulgent Genetics, |
RCV001780601 | SCV002815581 | pathogenic | Deficiency of steroid 17-alpha-monooxygenase | 2021-12-22 | criteria provided, single submitter | clinical testing | |
| Baylor Genetics | RCV001780601 | SCV004215443 | pathogenic | Deficiency of steroid 17-alpha-monooxygenase | 2024-03-06 | criteria provided, single submitter | clinical testing | |
| Prevention |
RCV003401710 | SCV004110119 | pathogenic | CYP17A1-related disorder | 2024-03-15 | no assertion criteria provided | clinical testing | The CYP17A1 c.1226C>G variant is predicted to result in the amino acid substitution p.Pro409Arg. This variant (also known as g.5582C>G) was reported in the compound heterozygous state in individuals with 17-alpha-hydroxylase deficiency (Lam et al 2001. PubMed ID: 11243732; Bee and Papari-Zareei. 2012. PubMed ID: 22087567). Functional studies also indicate this variant impacts 17-alpha-hydroxylase activity (Lam et al 2001. PubMed ID: 11243732; Han et al. 2013. PubMed ID: 23291414). This variant is reported in 0.030% of alleles in individuals of East Asian descent in gnomAD. This variant is interpreted as pathogenic. |