Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001551873 | SCV001772468 | pathogenic | not provided | 2021-05-20 | 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; Not observed in large population cohorts (Lek et al., 2016); This variant is associated with the following publications: (PMID: 27620904) |
Pittsburgh Clinical Genomics Laboratory, |
RCV004783937 | SCV005397710 | pathogenic | KBG syndrome | 2023-11-24 | criteria provided, single submitter | clinical testing | This sequence variant is a four-nucleotide deletion (delTGAG) in exon 9 of 13 of the ANKRD11 gene and results in an early termination signal 194 amino acids downstream of the frameshift at codon 1123. This variant is predicted to generate a non-functional allele through either the expression of a truncated protein or a loss of ankyrin repeat domain containing 11 expression due to nonsense mediated decay. This is a previously reported variant (ClinVar 978397) that has been observed in individuals affected by KGB syndrome (PMID: 27620904, 35970914). This variant is absent from the gnomAD v4 population database (0 of 833110 alleles). Haploinsufficiency in ANKRD11 is a known mechanism of disease (PMID: 29565525). Based upon the evidence, we consider this variant to be pathogenic. ACMG Criteria: PM2, PS4, PVS1 |
Service de Génétique Moléculaire, |
RCV001257006 | SCV001433562 | likely pathogenic | Rare genetic intellectual disability | no assertion criteria provided | clinical testing |