Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Hebei Industrial Technology Research Institute of Genomics in Maternal & Child Health, |
RCV003498013 | SCV004231838 | pathogenic | CHARGE syndrome | criteria provided, single submitter | clinical testing | The variant is detected as a de novo mutation in our trio pedigree, which is a stop-gain variant and causes protein truncation. The variant is graded as pathogenic (PVS1+PS2+PM2) referring to the ACMG criteria. It was also identified in two previous studies (PMID: 22461308 and PMID: 32625235). Besides, it is marked as disease mutation in HGMD (CM126591). However, this variant is not recorded in ClinVar. So we submit and suggest the variant to be recorded. | |
Labcorp Genetics |
RCV003498013 | SCV004295271 | pathogenic | CHARGE syndrome | 2023-03-29 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln136*) in the CHD7 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CHD7 are known to be pathogenic (PMID: 22461308, 25077900). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with clinical features of CHD7-related conditions (PMID: 22461308). For these reasons, this variant has been classified as Pathogenic. |