Total submissions: 6
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
The Laboratory of Genetics and Metabolism, |
RCV001009572 | SCV001169673 | pathogenic | Neurofibromatosis, type 1; Tibial pseudarthrosis | 2018-11-10 | criteria provided, single submitter | research | |
Labcorp Genetics |
RCV001381232 | SCV001579539 | pathogenic | Neurofibromatosis, type 1 | 2023-05-05 | 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: 818183). This premature translational stop signal has been observed in individual(s) with neurofibromatosis type 1 (PMID: 23913538). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Gln400*) 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). |
Gene |
RCV001593181 | SCV001824955 | pathogenic | not provided | 2021-12-07 | 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 (Lek 2016); This variant is associated with the following publications: (PMID: 15609345, 31370276, 30561760, 23913538, 31533797) |
Genome- |
RCV001381232 | SCV002561641 | pathogenic | Neurofibromatosis, type 1 | 2022-03-15 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002346210 | SCV002645197 | pathogenic | Hereditary cancer-predisposing syndrome; Cardiovascular phenotype | 2017-02-27 | criteria provided, single submitter | clinical testing | The p.Q400* pathogenic mutation (also known as c.1198C>T), located in coding exon 11 of the NF1 gene, results from a C to T substitution at nucleotide position 1198. This changes the amino acid from a glutamine to a stop codon within coding exon 11. This mutation was identified in 1/565 unrelated individuals making up a French NF1 cohort (Sabbagh A et al. Hum. Mutat. 2013 Nov;34:1510-8). 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. |
Eurofins- |
RCV001381232 | SCV003935062 | pathogenic | Neurofibromatosis, type 1 | 2022-09-12 | criteria provided, single submitter | clinical testing |