Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001882612 | SCV002245946 | pathogenic | not provided | 2024-05-24 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gly179Argfs*23) in the SLC45A2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SLC45A2 are known to be pathogenic (PMID: 21458243, 26573111). This variant is present in population databases (rs757344228, gnomAD 0.005%). This premature translational stop signal has been observed in individual(s) with oculocutaneous albinism (PMID: 34078970). ClinVar contains an entry for this variant (Variation ID: 1184503). For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV003394125 | SCV004120126 | pathogenic | SLC45A2-related disorder | 2022-12-09 | criteria provided, single submitter | clinical testing | The SLC45A2 c.533_534dupAG variant is predicted to result in a frameshift and premature protein termination (p.Gly179Argfs*23). This variant was reported in the heterozygous state along with a second plausible causative variant in individuals with oculocutaneous albinism (Kruijt et al. 2021. PubMed ID: 34078970). This variant is reported in 0.0046% of alleles in individuals of European (Non-Finnish) descent in gnomAD (http://gnomad.broadinstitute.org/variant/5-33982368-C-CCT). Frameshift variants in SLC45A2 are expected to be pathogenic. This variant is interpreted as pathogenic. |
Genomics England Pilot Project, |
RCV001542578 | SCV001760161 | pathogenic | Oculocutaneous albinism type 4 | no assertion criteria provided | clinical testing |