Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Blueprint Genetics | RCV000788837 | SCV000928097 | likely pathogenic | not provided | 2018-12-03 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV002535792 | SCV003516123 | pathogenic | Granulomatous disease, chronic, autosomal recessive, cytochrome b-positive, type 2 | 2024-11-04 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg184*) in the NCF2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in NCF2 are known to be pathogenic (PMID: 10498624, 20167518). This variant is present in population databases (rs766745748, gnomAD 0.003%). This premature translational stop signal has been observed in individual(s) with chronic granulomatous disease (PMID: 20167518, 30470980). ClinVar contains an entry for this variant (Variation ID: 636881). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV000788837 | SCV005080852 | pathogenic | not provided | 2024-04-22 | criteria provided, single submitter | clinical testing | Nonsense 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: 25525159, 20167518, 28251166, 30470980, 32441320, 33365035, 33717137) |