Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Fulgent Genetics, |
RCV001535979 | SCV001752646 | pathogenic | Amelogenesis imperfecta type 1G | 2024-06-17 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV002546414 | SCV003442410 | pathogenic | not provided | 2022-09-13 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site. ClinVar contains an entry for this variant (Variation ID: 1029473). This premature translational stop signal has been observed in individual(s) with clinical features of enamel renal syndrome (PMID: 23434854). This variant is present in population databases (rs760163489, gnomAD 0.004%). This sequence change creates a premature translational stop signal (p.Phe305Leufs*76) in the FAM20A gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in FAM20A are known to be pathogenic (PMID: 21990045, 23434854). |
Genomic Medicine Center of Excellence, |
RCV001535979 | SCV004805352 | pathogenic | Amelogenesis imperfecta type 1G | 2024-03-25 | criteria provided, single submitter | research | |
Gene |
RCV002546414 | SCV005689888 | pathogenic | not provided | 2024-08-06 | criteria provided, single submitter | clinical testing | Frameshift variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; This variant is associated with the following publications: (PMID: 28298625, 37228816, 37159186, 32835847, 21990045, 24927635, 23434854) |
Clinical Laboratory Sciences Program |
RCV001535979 | SCV003927870 | pathogenic | Amelogenesis imperfecta type 1G | 2023-04-01 | no assertion criteria provided | clinical testing |