Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000808377 | SCV000948485 | pathogenic | Neurofibromatosis, type 1 | 2024-12-20 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 2 of the NF1 gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and 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). Disruption of this splice site has been observed in individuals with juvenile myelomonocytic leukemia (JMML) and/or neurofibromatosis type 1 (NF1) (PMID: 22155606, 23222849; internal data). ClinVar contains an entry for this variant (Variation ID: 652752). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV001585736 | SCV001813809 | pathogenic | not provided | 2021-01-06 | criteria provided, single submitter | clinical testing | Canonical splice site variant expected to result in aberrant splicing, although in the absence of functional evidence the actual effect of this sequence change is unknown.; Deletions involving coding exons of this gene are a known mechanism of disease (Stenson et al., 2014); Not observed in large population cohorts (Lek et al., 2016); This variant is associated with the following publications: (PMID: 24077912, 23913538, 23222849, 22155606) |
Genome- |
RCV000808377 | SCV002561556 | pathogenic | Neurofibromatosis, type 1 | 2022-03-15 | criteria provided, single submitter | clinical testing |