Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV003596842 | SCV004293799 | pathogenic | Congenital factor V deficiency | 2024-01-25 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg1030*) in the F5 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in F5 are known to be pathogenic (PMID: 30924984). This variant is present in population databases (rs780253174, gnomAD 0.006%). This premature translational stop signal has been observed in individual(s) with clinical features of factor V deficiency (PMID: 12816860, 31399523). This variant is also known as p.Arg1002ter. For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV004753692 | SCV005365492 | likely pathogenic | F5-related disorder | 2024-08-23 | no assertion criteria provided | clinical testing | The F5 c.3088C>T variant is predicted to result in premature protein termination (p.Arg1030*). This variant was reported in the compound heterozygous state in an individual with Factor V deficiency (Reported as p.Arg1002* in Patient 6, Montefusco et al. 2003. PubMed ID: 12816860). This variant is reported in 0.0065% of alleles in individuals of South Asian descent in gnomAD. Nonsense variants in F5 are expected to be pathogenic. This variant is interpreted as likely pathogenic. |