Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000434287 | SCV000524588 | pathogenic | not provided | 2023-03-24 | criteria provided, single submitter | clinical testing | Reported in the homozygous state in an individual with a clinical diagnosis of Leber congenital amaurosis in published literature, although this individual was also homozygous for a frameshift variant in the PLA2G6 gene (Soens et al., 2017); Published functional studies demonstrate abnormal gene splicing (Soens et al., 2017); This variant is associated with the following publications: (PMID: 28714225, 33594928, 35029636) |
Labcorp Genetics |
RCV000434287 | SCV003443633 | uncertain significance | not provided | 2022-10-13 | criteria provided, single submitter | clinical testing | This sequence change falls in intron 2 of the SLC38A8 gene. It does not directly change the encoded amino acid sequence of the SLC38A8 protein. It affects a nucleotide within the consensus splice site. This variant is present in population databases (rs760391436, gnomAD 0.006%). This variant has been observed in individual(s) with foveal hypoplasia (PMID: 33594928). ClinVar contains an entry for this variant (Variation ID: 383962). Variants that disrupt the consensus splice site are a relatively common cause of aberrant splicing (PMID: 17576681, 9536098). Studies have shown that this variant alters mRNA splicing and is expected to lead to the loss of protein expression (PMID: 28714225). In summary, the available evidence is currently insufficient to determine the role of this variant in disease. Therefore, it has been classified as a Variant of Uncertain Significance. |
Rui Chen Lab, |
RCV000515654 | SCV000579411 | likely pathogenic | Leber congenital amaurosis | 2017-05-09 | no assertion criteria provided | research |