Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Laboratory for Molecular Medicine, |
RCV000024036 | SCV001653012 | pathogenic | Microcephaly 2, primary, autosomal recessive, with or without cortical malformations | 2020-06-08 | criteria provided, single submitter | clinical testing | The p.Gln918GlyfsX18 variant WDR62 has been reported in 2 siblings with autosomal recessive microcephaly/polymicrogyria in a compound heterozygous state with another frameshift variant (Murdock 2011 PMID: 21834044). It was also identified in 1/113224 of European chromosomes by gnomAD (http://gnomad.broadinstitute.org). This variant is predicted to cause a frameshift, which alters the protein’s amino acid sequence beginning at position 918 and leads to a premature termination codon 18 amino acids downstream. This alteration is then predicted to lead to a truncated or absent protein. Loss of function of the WDR62 gene is strongly associated with autosomal recessive primary microcephaly/polymicrogyria. In summary, this variant meets criteria to be classified as pathogenic for autosomal recessive primary microcephaly. ACMG/AMP Criteria applied: PM2, PVS1, PP1, PM3. |
Revvity Omics, |
RCV000024036 | SCV002020901 | pathogenic | Microcephaly 2, primary, autosomal recessive, with or without cortical malformations | 2021-01-08 | criteria provided, single submitter | clinical testing | |
Gene |
RCV003229803 | SCV003927500 | pathogenic | not provided | 2023-05-23 | 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 at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 21834044) |
OMIM | RCV000024036 | SCV000045327 | pathogenic | Microcephaly 2, primary, autosomal recessive, with or without cortical malformations | 2011-09-01 | no assertion criteria provided | literature only |