Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
UAB Medical Genomics Laboratory, |
RCV001007750 | SCV001167429 | pathogenic | Neurofibromatosis, type 1 | 2020-01-20 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001007750 | SCV002254854 | pathogenic | Neurofibromatosis, type 1 | 2022-08-31 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Studies have shown that this variant results in activation of a cryptic splice site and introduces a premature termination codon (PMID: 32126153). The resulting mRNA is expected to undergo nonsense-mediated decay. ClinVar contains an entry for this variant (Variation ID: 561680). This variant has been observed in individual(s) with clinical features of neurofibromatosis type 1 and/or neurofibromatosis type 1 (PMID: 32126153; Invitae). In at least one individual the variant was observed to be de novo. This variant is not present in population databases (gnomAD no frequency). This sequence change falls in intron 36 of the NF1 gene. It does not directly change the encoded amino acid sequence of the NF1 protein. RNA analysis indicates that this variant induces altered splicing and may result in an absent or disrupted protein product. |
MGZ Medical Genetics Center | RCV001007750 | SCV002581707 | likely pathogenic | Neurofibromatosis, type 1 | 2022-08-08 | criteria provided, single submitter | clinical testing | |
Institute of Human Genetics, |
RCV001007750 | SCV004027713 | likely pathogenic | Neurofibromatosis, type 1 | 2023-07-03 | criteria provided, single submitter | clinical testing | Criteria applied: PS3_MOD,PS4_MOD,PM2_SUP,PP3,PP4 |
Gene |
RCV000681028 | SCV000808480 | uncertain significance | not provided | 2018-08-10 | flagged submission | clinical testing | The c.5206-14 C>G variant has not been published as a pathogenic variant, nor has it been reported as a benign variant to our knowledge. The variant is not observed in large population cohorts (Lek et al., 2016). Several in silico splice prediction models predict that c.5206-14 C>G creates a cryptic acceptor site which may supplant the natural acceptor site and lead to abnormal gene splicing. However, in the absence of RNA/functional studies, the actual effect of this sequence change in this individual is unknown. Therefore, based on the currently available information, it is unclear whether this variant is a pathogenic variant or a rare benign variant. |