Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001008105 | SCV001167855 | pathogenic | not provided | 2020-12-01 | criteria provided, single submitter | clinical testing | Frameshift 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 a significant frequency in large population cohorts (Lek 2016); Identified in patients with a personal or family history consistent with pathogenic variants in this gene referred for genetic testing at GeneDx and in published literature (Ars 2003, Pros 2008, Giugliano 2019); This variant is associated with the following publications: (PMID: 12807981, 31370276, 31201679, 18546366) |
Labcorp Genetics |
RCV001381233 | SCV001579541 | pathogenic | Neurofibromatosis, type 1 | 2024-09-23 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Thr467Asnfs*3) 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 present in population databases (rs778963145, gnomAD 0.003%). This premature translational stop signal has been observed in individual(s) with neurofibromatosis type 1 (PMID: 12807981, 31201679, 31370276). ClinVar contains an entry for this variant (Variation ID: 817038). For these reasons, this variant has been classified as Pathogenic. |
Genome- |
RCV001381233 | SCV002561663 | pathogenic | Neurofibromatosis, type 1 | 2022-03-15 | criteria provided, single submitter | clinical testing |