Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000638440 | SCV000759955 | pathogenic | Kabuki syndrome | 2017-09-06 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Tyr2199Ilefs*65) in the KMT2D gene. It is expected to result in an absent or disrupted protein product. This variant is not present in population databases (ExAC no frequency). This variant has been reported in the literature in an individual affected with Kabuki syndrome (PMID: 21671394). Loss-of-function variants in KMT2D are known to be pathogenic (PMID: 22126750). For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV004758713 | SCV005344160 | pathogenic | KMT2D-related disorder | 2024-04-04 | no assertion criteria provided | clinical testing | The KMT2D c.6594delC variant is predicted to result in a frameshift and premature protein termination (p.Tyr2199Ilefs*65). This variant was reported in an individual with Kabuki syndrome (Table S2, Hannibal et al. 2011. PubMed ID: 21671394). This variant has not been reported in a large population database, indicating this variant is rare. Frameshift variants in KMT2D are expected to be pathogenic. This variant is interpreted as pathogenic. |