Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Clin |
RCV000106358 | SCV001146734 | pathogenic | Phenylketonuria | 2019-05-26 | reviewed by expert panel | curation | The c.504C>A (p.Tyr168Ter) variant in PAH has been previously reported in one proband with mild hyperphenylalanemia (PMID: 26666653; PP4). The proband was said to be heterozygous for the variant and also harbor the known pathogenic allele (per ClinGen PAH VCEP, see ClinVar ID 92751) c.898G>T (p.Ala300Ser); however, the phase of the variants was not confirmed via parental testing (PM3_supporting). The sequence change results in a nonsense variant which occurs in exon 5 of 13 in the in the canonical transcript of PAH, a gene fulfilling the most recent criteria for LOF being a known disease mechanism (see PMID: 30192042) (PVS1). It is absent from control databases (PM2). In summary, this variant meets criteria to be classified as pathogenic for PAH. PAH-specific ACMG/AMP criteria applied: PVS1, PM2, PP4, PM3_supporting. |
Labcorp Genetics |
RCV000106358 | SCV001407822 | pathogenic | Phenylketonuria | 2019-10-15 | criteria provided, single submitter | clinical testing | Loss-of-function variants in PAH are known to be pathogenic (PMID: 1301187, 9634518). This variant has been observed in an individual affected with hyperphenylalaninemia (PMID: 26666653). ClinVar contains an entry for this variant (Variation ID: 120277). This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Tyr168*) in the PAH gene. It is expected to result in an absent or disrupted protein product. For these reasons, this variant has been classified as Pathogenic. |
Inserm U 954, |
RCV000106358 | SCV000143857 | probable-pathogenic | Phenylketonuria | no assertion criteria provided | not provided | Converted during submission to Likely pathogenic. |