Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Genome Diagnostics Laboratory, |
RCV001290779 | SCV001478915 | pathogenic | Neurofibromatosis, type 1 | 2020-10-26 | criteria provided, single submitter | clinical testing | |
Human Genetics Bochum, |
RCV001290779 | SCV002758611 | pathogenic | Neurofibromatosis, type 1 | 2021-12-06 | criteria provided, single submitter | clinical testing | ACMG criteria used to clasify this variant: PVS1, PM4, PM2 |
Gene |
RCV003442822 | SCV004169405 | pathogenic | not provided | 2023-05-10 | 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 significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 31370276, 23913538) |
Labcorp Genetics |
RCV001290779 | SCV004297465 | pathogenic | Neurofibromatosis, type 1 | 2023-08-16 | 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: 996375). This premature translational stop signal has been observed in individual(s) with clinical features of 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.Asp1116Alafs*25) 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). |
Laboratory of Medical Genetics, |
RCV001290779 | SCV001548492 | pathogenic | Neurofibromatosis, type 1 | 2020-01-01 | no assertion criteria provided | clinical testing |