Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Center for Individualized Medicine, |
RCV000190643 | SCV000245686 | likely pathogenic | Fanconi anemia complementation group I | 2014-01-01 | criteria provided, single submitter | research | |
Labcorp Genetics |
RCV000630839 | SCV000751808 | pathogenic | Fanconi anemia | 2024-01-16 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Lys808*) in the FANCI gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in FANCI are known to be pathogenic (PMID: 17452773, 17460694). This variant is present in population databases (rs375656231, gnomAD 0.002%). This premature translational stop signal has been observed in individual(s) with breast or prostate cancer (PMID: 26296701, 29439820). ClinVar contains an entry for this variant (Variation ID: 208639). 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. |
Daryl Scott Lab, |
RCV000190643 | SCV001448633 | pathogenic | Fanconi anemia complementation group I | 2020-11-11 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV000190643 | SCV004197221 | likely pathogenic | Fanconi anemia complementation group I | 2024-03-01 | criteria provided, single submitter | clinical testing |