Total submissions: 7
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000803171 | SCV000943033 | pathogenic | Familial aplasia of the vermis; Meckel-Gruber syndrome; Nephronophthisis | 2023-07-31 | 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: 99861). This premature translational stop signal has been observed in individual(s) with Leber congenital amaurosis (LCA) (PMID: 16909394, 17705300, 20690115, 21153841). The frequency data for this variant in the population databases is considered unreliable, as metrics indicate poor data quality at this position in the gnomAD database. This sequence change creates a premature translational stop signal (p.Thr1938Asnfs*16) in the CEP290 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CEP290 are known to be pathogenic (PMID: 16909394, 17345604, 20690115). |
Ce |
RCV000086299 | SCV001246562 | pathogenic | not provided | 2018-11-01 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV002505021 | SCV002810450 | pathogenic | Leber congenital amaurosis 10; Meckel syndrome, type 4; Senior-Loken syndrome 6; Joubert syndrome 5; Bardet-Biedl syndrome 14 | 2022-03-11 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV003467016 | SCV004214878 | pathogenic | Bardet-Biedl syndrome 14 | 2023-12-19 | criteria provided, single submitter | clinical testing | |
Retina International | RCV000086299 | SCV000118445 | not provided | not provided | no assertion provided | not provided | ||
Natera, |
RCV001826776 | SCV002091861 | pathogenic | Leber congenital amaurosis | 2021-02-05 | no assertion criteria provided | clinical testing | |
Prevention |
RCV004529903 | SCV004121514 | pathogenic | CEP290-related disorder | 2024-09-11 | no assertion criteria provided | clinical testing | The CEP290 c.5813_5817del5 variant is predicted to result in a frameshift and premature protein termination (p.Thr1938Asnfs*16). This variant has been reported in the compound heterozygous state with a recurrent deep intronic variant (c.2991+1655A>G) in multiple individuals with Leber Congenital Amaurosis (den Hollander et al. 2006. PubMed ID: 16909394; Frank et al. 2008. PubMed ID: 17705300; Wiszniewski et al. 2011. PubMed ID: 21153841; Testa et al. 2021. PubMed ID: 34196655). This variant is reported in 0.00081% of alleles in individuals of European (Non-Finnish) descent in gnomAD. Frameshift variants in CEP290 are expected to be pathogenic. Given the evidence, we interpret c.5813_5817del (p.Thr1938Asnfs*16) as pathogenic. |