Total submissions: 8
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000003613 | SCV000486649 | pathogenic | Fanconi anemia complementation group A | 2016-11-02 | criteria provided, single submitter | clinical testing | |
Invitae | RCV000630905 | SCV000751878 | pathogenic | Fanconi anemia | 2023-12-16 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg1187Glufs*28) in the FANCA gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in FANCA are known to be pathogenic (PMID: 19367192). This variant is present in population databases (rs747851434, gnomAD 0.005%). This premature translational stop signal has been observed in individual(s) with Fanconi anemia (PMID: 9399890, 17924555, 24584348). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. ClinVar contains an entry for this variant (Variation ID: 3444). For these reasons, this variant has been classified as Pathogenic. |
Genetic Services Laboratory, |
RCV001818121 | SCV002072231 | pathogenic | not provided | 2021-01-12 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001818121 | SCV002504446 | pathogenic | not provided | 2022-04-11 | 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; Reported in ClinVar as pathogenic (ClinVar Variant ID# 3444; ClinVar); This variant is associated with the following publications: (PMID: 10431244, 17924555, 9399890, 31589614, 33718801, 24584348) |
Prevention |
RCV003398432 | SCV004119271 | pathogenic | FANCA-related disorder | 2023-09-15 | criteria provided, single submitter | clinical testing | The FANCA c.3558dupG variant is predicted to result in a frameshift and premature protein termination (p.Arg1187Glufs*28). In the literature this variant is also referred to as c.3559insG and c.3558_3559insG. This variant has been reported in the homozygous and presumed compound heterozygous states in individuals with Fanconi anemia (Savino et al. 1997. PubMed ID: 9399890; Ameziane et al. 2008. PubMed ID: 17924555). This variant is reported in 0.0047% of alleles in individuals of European (Non-Finnish) descent in gnomAD (http://gnomad.broadinstitute.org/variant/16-89811434-T-TC). Frameshift variants in FANCA are expected to be pathogenic. This variant is interpreted as pathogenic. |
Baylor Genetics | RCV000003613 | SCV004196554 | pathogenic | Fanconi anemia complementation group A | 2024-03-18 | criteria provided, single submitter | clinical testing | |
OMIM | RCV000003613 | SCV000023771 | pathogenic | Fanconi anemia complementation group A | 1999-08-01 | no assertion criteria provided | literature only | |
Natera, |
RCV000003613 | SCV001458758 | pathogenic | Fanconi anemia complementation group A | 2020-09-16 | no assertion criteria provided | clinical testing |