Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000460781 | SCV000546476 | pathogenic | Hypertrophic cardiomyopathy | 2024-05-22 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Tyr79*) in the MYBPC3 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in MYBPC3 are known to be pathogenic (PMID: 19574547). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with hypertrophic cardiomyopathy (PMID: 19574547, 23140321, 24510615). ClinVar contains an entry for this variant (Variation ID: 407333). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV000483607 | SCV000573944 | pathogenic | not provided | 2017-03-14 | criteria provided, single submitter | clinical testing | The Y79X (c.237 C>A) variant in the MYBPC3 gene has been reported in at least 3 individuals with confirmedhypertrophic cardiomyopathy (HCM) or who were referred for HCM gene testing (Kapplinger et al., 2014; Bos et al.,2014). This variant is predicted to cause loss of normal protein function either by protein truncation or nonsensemediatedmRNA decay. Other nonsense variants in the MYBPC3 gene, including a different nonsense variant at thesame residue (c.237 C>G), have been reported in Human Gene Mutation Database in association with HCM (Stensonet al., 2014), indicating that loss of function is a known disease mechanism. Finally, the Y79X (c.237 C>A) variantis not observed in large population cohorts (Lek et al., 2016; 1000 Genomes Consortium et al., 2015; Exome VariantServer). |