Total submissions: 1
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001914784 | SCV002138156 | pathogenic | Neurofibromatosis, type 1 | 2021-10-02 | criteria provided, single submitter | clinical testing | This variant disrupts a region of the NF1 protein in which other variant(s) (p.Arg1000Pro) have been determined to be pathogenic (Invitae). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. For these reasons, this variant has been classified as Pathogenic. Variants that disrupt the consensus splice site are a relatively common cause of aberrant splicing (PMID: 17576681, 9536098). Studies have shown that this missense change results in skipping of exon 23 (also called exon 18), but is expected to preserve the integrity of the reading-frame (PMID: 18546366). This sequence change replaces arginine with threonine at codon 1038 of the NF1 protein (p.Arg1038Thr). The arginine residue is moderately conserved and there is a moderate physicochemical difference between arginine and threonine. RNA analysis indicates that this missense change induces altered splicing and likely results in a shortened protein product. This variant is not present in population databases (ExAC no frequency). This missense change has been observed in individual(s) with clinical features of neurofibromatosis type 1 (PMID: 18546366). Algorithms developed to predict the effect of missense changes on protein structure and function are either unavailable or do not agree on the potential impact of this missense change (SIFT: "Deleterious"; PolyPhen-2: "Probably Damaging"; Align-GVGD: "Class C0"). |