Total submissions: 5
| Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
|---|---|---|---|---|---|---|---|---|
| Wessex Regional Genetics Laboratory, |
RCV000856851 | SCV000999399 | pathogenic | Rubinstein-Taybi syndrome due to CREBBP mutations | 2019-11-05 | criteria provided, single submitter | clinical testing | |
| Equipe Genetique des Anomalies du Developpement, |
RCV001526626 | SCV001737056 | pathogenic | Corpus callosum, agenesis of | criteria provided, single submitter | clinical testing | ||
| Illumina Laboratory Services, |
RCV000856851 | SCV002540225 | pathogenic | Rubinstein-Taybi syndrome due to CREBBP mutations | 2021-12-15 | criteria provided, single submitter | clinical testing | The CREBBP c.1108C>T (p.Arg370Ter) nonsense variant results in the substitution of arginine at amino acid position 370 with a stop codon. Loss of normal protein function through either protein truncation or nonsense-mediated mRNA decay is expected. This variant has been reported in a heterozygous state in at least seven individuals with Rubinstein-Taybi syndrome, including in a presumed de novo state in at least two individuals (Coupry et al. 2002; Bartsch et al. 2002; Udaka et al. 2005; Bentivengna et al. 2006; Cross et al. 2020; Squeo et al. 2020). The c.1108C>T 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.1108C>T (p.Arg370Ter) variant is classified as pathogenic for Rubinstein-Taybi syndrome. |
| Equipe Genetique des Anomalies du Developpement, |
RCV000856851 | SCV003843210 | pathogenic | Rubinstein-Taybi syndrome due to CREBBP mutations | 2021-02-26 | criteria provided, single submitter | clinical testing | |
| Labcorp Genetics |
RCV005092540 | SCV005838412 | pathogenic | Rubinstein-Taybi syndrome | 2024-04-24 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg370*) in the CREBBP gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CREBBP are known to be pathogenic (PMID: 17052327, 18792986). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with Rubinstein-Taybi syndrome (PMID: 32170002, 32827181). ClinVar contains an entry for this variant (Variation ID: 694759). For these reasons, this variant has been classified as Pathogenic. |