Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001387788 | SCV001588505 | pathogenic | Neurofibromatosis, type 1 | 2023-01-21 | 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: 1074475). This premature translational stop signal has been observed in individual(s) with clinical features of neurofibromatosis type 1 (PMID: 26740943). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Ser2540*) in the NF1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in NF1 are known to be pathogenic (PMID: 10712197, 23913538). |
ARUP Laboratories, |
RCV003738059 | SCV004564284 | pathogenic | not provided | 2022-12-29 | criteria provided, single submitter | clinical testing | The NF1 c.7682C>G; p.Ser2561Ter variant (also known as NM_000267.3: c.7619C>G p.Ser2540Ter) is reported in the literature in an individual with neurofibromatosis type 1 (Bianchessi 2015). This variant is also reported in ClinVar (Variation ID: 1074475). It is absent from the Genome Aggregation Database, indicating it is not a common polymorphism. This variant induces an early termination codon and is predicted to result in a truncated protein or mRNA subject to nonsense-mediated decay. Based on available information, this variant is considered to be pathogenic. References: Bianchessi D et al. 126 novel mutations in Italian patients with neurofibromatosis type 1. Mol Genet Genomic Med. 2015 Jul 7;3(6):513-25. PMID: 26740943. |
Gene |
RCV003738059 | SCV005325961 | pathogenic | not provided | 2024-01-05 | criteria provided, single submitter | clinical testing | Identified in patients with features of NF1 referred for genetic testing at GeneDx and in published literature (PMID: 26740943, 31766501); Not observed at significant frequency in large population cohorts (gnomAD); 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; This variant is associated with the following publications: (PMID: 26740943, 36625737, 31766501) |