Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001946976 | SCV002242759 | pathogenic | Immunodeficiency, common variable, 2 | 2023-08-04 | 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: 1456816). This premature translational stop signal has been observed in individual(s) with common variable immunodeficiency (PMID: 18981294). This variant is present in population databases (rs774205573, gnomAD 0.003%). This sequence change creates a premature translational stop signal (p.Cys100Leufs*6) in the TNFRSF13B gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in TNFRSF13B are known to be pathogenic (PMID: 16007087, 27123465). |
Prevention |
RCV003941225 | SCV004754852 | likely pathogenic | TNFRSF13B-related disorder | 2024-02-29 | no assertion criteria provided | clinical testing | The TNFRSF13B c.298dupT variant is predicted to result in a frameshift and premature protein termination (p.Cys100Leufs*6). This variant was reported in the heterozygous state along with a second variant on the same allele (c.121G>C, p.Asp41His) in one individual with common variable immunodeficiency disorder (CVID) as well as two unaffected family members (Salzer et al. 2009. PubMed ID: 18981294). This variant is reported in 0.0058% of alleles in individuals of Latino descent in gnomAD. Frameshift variants in TNFRSF13B are expected to be pathogenic. This variant is interpreted as likely pathogenic. |