Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV000492570 | SCV000580749 | pathogenic | Hereditary cancer-predisposing syndrome | 2019-09-17 | criteria provided, single submitter | clinical testing | The c.1213dupT pathogenic mutation, located in coding exon 8 of the FLCN gene, results from a duplication of T at nucleotide position 1213, causing a translational frameshift with a predicted alternate stop codon (p.Y405Lfs*51). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |
Labcorp Genetics |
RCV000817465 | SCV000958027 | pathogenic | Birt-Hogg-Dube syndrome | 2022-11-24 | criteria provided, single submitter | clinical testing | This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Tyr405Leufs*51) in the FLCN gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in FLCN are known to be pathogenic (PMID: 15852235). ClinVar contains an entry for this variant (Variation ID: 428651). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site. This variant has not been reported in the literature in individuals affected with FLCN-related conditions. For these reasons, this variant has been classified as Pathogenic. |