Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV000574913 | SCV000673465 | pathogenic | Hereditary cancer-predisposing syndrome | 2016-12-08 | criteria provided, single submitter | clinical testing | The c.1153delC pathogenic mutation, located in coding exon 7 of the FLCN gene, results from a deletion of one nucleotide at nucleotide position 1153, causing a translational frameshift with a predicted alternate stop codon (p.Q385Sfs*83). 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 |
RCV005091424 | SCV005741197 | pathogenic | Birt-Hogg-Dube syndrome | 2024-03-30 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln385Serfs*83) 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). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with renal cancer (PMID: 32782288). ClinVar contains an entry for this variant (Variation ID: 485603). For these reasons, this variant has been classified as Pathogenic. |