Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Division Of Personalized Genomic Medicine, |
RCV000851562 | SCV004037366 | pathogenic | Fanconi anemia complementation group B | 2020-10-19 | criteria provided, single submitter | clinical testing | The c.1668delT variant is a heterozygous single-base deletion in exon 8 (out of 10 exons) of the FANCB (NM_001018113.3) gene. It causes a frameshift at amino acid position 557, changing aspartic acid at this position to isoleucine and resulting in a premature stop codon 21 residues downstream (p.Asp557Ilefs*21). This variant is predicted to cause loss-of-function of the protein by nonsense mediated mRNA decay. It is absent in the Genome Aggregation Database (gnomAD), indicating that it is not a common benign variant in the populations represented therein. This variant in hemizygous state has been previously reported as 1650delT in a male patient with Fanconi anemia complementation group B (PMID: 15502827 and 17924555). It has also been reported in the ClinVar database as pathogenic by two submitters (Variation ID: 562389, last accessed 10/19/2020). Based on these reasons, it is classified here as a pathogenic variant. |
OMIM | RCV000851562 | SCV000031847 | pathogenic | Fanconi anemia complementation group B | 2004-11-01 | no assertion criteria provided | literature only | |
Gharavi Laboratory, |
RCV000681853 | SCV000809331 | pathogenic | not provided | 2018-09-16 | no assertion criteria provided | research | |
Leiden Open Variation Database | RCV000851562 | SCV000994636 | pathogenic | Fanconi anemia complementation group B | 2020-02-28 | no assertion criteria provided | curation | Curator: Arleen D. Auerbach. Submitters to LOVD: Arleen D. Auerbach, Johan de Winter. |