Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000480025 | SCV000568258 | pathogenic | not provided | 2019-08-05 | criteria provided, single submitter | clinical testing | Nonsense variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss-of-function is a known mechanism of disease; Not observed in large population cohorts (Lek et al., 2016); This variant is associated with the following publications: (PMID: 23365099) |
Illumina Laboratory Services, |
RCV003315243 | SCV004014847 | pathogenic | Lissencephaly type 1 due to doublecortin gene mutation | 2023-03-10 | criteria provided, single submitter | clinical testing | The DCX c.505C>T (p.Gln169Ter) nonsense variant results in a premature termination of the protein at amino acid position 169. This variant is also known as c.748C>T (p.Gln250Ter) on NM_000555.3. Loss of normal protein function through either protein truncation or nonsense-mediated mRNA decay is expected. This variant has been reported in a de novo state in a 15-year-old with intellectual disability, autism, and subcortical band heterotopia (PMID: 23365099). The p.Gln169Ter variant is not found in version 2.1.1 or version 3.1.2 of the Genome Aggregation Database. This variant was identified in a de novo state. Based on the available evidence, the c.505C>T (p.Gln169Ter) variant is classified as pathogenic for lissencephaly spectrum disorders. |