Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001769362 | SCV002001216 | uncertain significance | not provided | 2020-12-21 | criteria provided, single submitter | clinical testing | In silico analysis supports that this missense variant has a deleterious effect on protein structure/function; Has not been previously published as pathogenic or benign to our knowledge |
Labcorp Genetics |
RCV001868605 | SCV002145962 | likely benign | Kabuki syndrome | 2023-10-05 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV004040274 | SCV004896615 | uncertain significance | Inborn genetic diseases | 2024-01-02 | criteria provided, single submitter | clinical testing | The c.6223A>C (p.K2075Q) alteration is located in exon 30 (coding exon 30) of the KMT2D gene. This alteration results from a A to C substitution at nucleotide position 6223, causing the lysine (K) at amino acid position 2075 to be replaced by a glutamine (Q). Based on insufficient or conflicting evidence, the clinical significance of this alteration remains unclear. |
Prevention |
RCV004758827 | SCV005362755 | uncertain significance | KMT2D-related disorder | 2024-05-31 | no assertion criteria provided | clinical testing | The KMT2D c.6223A>C variant is predicted to result in the amino acid substitution p.Lys2075Gln. To our knowledge, this variant has not been reported in the literature. This variant is reported in 0.0029% of alleles in individuals of Latino descent in gnomAD. At this time, the clinical significance of this variant is uncertain due to the absence of conclusive functional and genetic evidence. |