Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001047337 | SCV001211287 | likely pathogenic | not provided | 2023-12-06 | criteria provided, single submitter | clinical testing | This sequence change affects a donor splice site in intron 5 of the TYMP 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 TYMP are known to be pathogenic (PMID: 9924029, 15781193). This variant is present in population databases (rs760629248, gnomAD 0.003%). Disruption of this splice site has been observed in individual(s) with mitochondrial neurogastrointestinal encephalomyopathy (PMID: 19523753). This variant is also known as c.130G>A or IVS5+1G>A. ClinVar contains an entry for this variant (Variation ID: 844485). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. 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. |
Baylor Genetics | RCV003467749 | SCV004207529 | pathogenic | Mitochondrial DNA depletion syndrome 1 | 2023-11-27 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001047337 | SCV005201504 | pathogenic | not provided | 2023-10-26 | criteria provided, single submitter | clinical testing | Canonical splice site variant predicted to result in a null allele in a gene for which loss of function is a known mechanism of disease; Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 25525159, 19523753) |