Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000523090 | SCV000618451 | pathogenic | not provided | 2017-07-18 | criteria provided, single submitter | clinical testing | The Y760X variant in the TBCD gene has been reported previously in the compound heterozygous state with a second TBCD variant in association with early-onset neurodegenerative encephalopathy (Miyake et al., 2016). This variant is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. The Y760X variant is not observed in large population cohorts (Lek et al., 2016; 1000 Genomes Consortium et al., 2015; Exome Variant Server). We interpret Y760X as a pathogenic variant. |
Labcorp Genetics |
RCV000523090 | SCV004296899 | pathogenic | not provided | 2023-06-20 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 268170). This premature translational stop signal has been observed in individual(s) with early-onset neurodegenerative encephalopathy (PMID: 27666374). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Tyr760*) in the TBCD gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in TBCD are known to be pathogenic (PMID: 27666370, 27666374). |
OMIM | RCV000258906 | SCV000328659 | pathogenic | Early-onset progressive diffuse brain atrophy-microcephaly-muscle weakness-optic atrophy syndrome | 2016-11-16 | no assertion criteria provided | literature only |