Total submissions: 6
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000206167 | SCV000260771 | pathogenic | Neurofibromatosis, type 1 | 2023-05-11 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln1820*) 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). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with neurofibromatosis 1 (PMID: 10090487). ClinVar contains an entry for this variant (Variation ID: 220317). For these reasons, this variant has been classified as Pathogenic. |
Genome Diagnostics Laboratory, |
RCV000206167 | SCV001479016 | pathogenic | Neurofibromatosis, type 1 | 2020-10-26 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001824299 | SCV002073984 | pathogenic | not provided | 2024-04-02 | 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 at significant frequency in large population cohorts (gnomAD); Also known as c.5458C>T; p.Gln1828X; This variant is associated with the following publications: (PMID: 23404336, 10712197, 25525159, 10090487, 23913538, 22190595, 31573083) |
Genome- |
RCV000206167 | SCV002560127 | pathogenic | Neurofibromatosis, type 1 | 2022-03-15 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002345737 | SCV002649721 | pathogenic | Hereditary cancer-predisposing syndrome; Cardiovascular phenotype | 2021-05-20 | criteria provided, single submitter | clinical testing | The p.Q1820* pathogenic mutation (also known as c.5458C>T), located in coding exon 37 of the NF1 gene, results from a C to T substitution at nucleotide position 5458. This changes the amino acid from a glutamine to a stop codon within coding exon 37. This alteration has been reported in individuals meeting diagnostic criteria for neurofibromatosis type 1 (NF1) or with NF1 features (Peters H et al. Hum. Mutat., 1999;13:258; Ribeiro MJ et al. Invest Ophthalmol Vis Sci, 2012 Jan;53:287-93; Violante IR et al. Brain, 2013 Mar;136:918-25; Castellanos E et al. Clin Genet, 2020 02;97:264-275). In addition to the clinical data presented in the literature, this alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |
Zotz- |
RCV000206167 | SCV004101045 | likely pathogenic | Neurofibromatosis, type 1 | 2023-11-02 | no assertion criteria provided | clinical testing |