Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute for Medical Genetics and Human Genetics, |
RCV001450018 | SCV001653567 | pathogenic | Greig cephalopolysyndactyly syndrome | 2021-06-01 | criteria provided, single submitter | research | |
Mendelics | RCV002246386 | SCV002516492 | pathogenic | Pallister-Hall syndrome | 2022-05-04 | criteria provided, single submitter | clinical testing | |
Gene |
RCV002265029 | SCV002547064 | pathogenic | not provided | 2022-01-05 | criteria provided, single submitter | clinical testing | Nonsense 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; This variant is associated with the following publications: (PMID: 34638259, 25525159, 33502061, 34482537, 31502745) |
Ambry Genetics | RCV003264039 | SCV003970703 | pathogenic | Inborn genetic diseases | 2023-05-19 | criteria provided, single submitter | clinical testing | The c.1999C>T (p.R667*) alteration, located in exon 13 (coding exon 12) of the GLI3 gene, consists of a C to T substitution at nucleotide position 1999. This changes the amino acid from a arginine (R) to a stop codon at amino acid position 667. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. This allele was reported in one heterozygous individual in population-based cohorts in the Genome Aggregation Database (gnomAD). This variant has been reported in a family with features consistent with GLI3-related digital anomaly disorders (Sczakiel, 2021). Based on the available evidence, this alteration is classified as pathogenic. |