Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000635192 | SCV000756570 | benign | Early myoclonic encephalopathy | 2025-01-22 | criteria provided, single submitter | clinical testing | |
Breakthrough Genomics, |
RCV004712913 | SCV005267025 | benign | not provided | criteria provided, single submitter | not provided | ||
Women's Health and Genetics/Laboratory Corporation of America, |
RCV005240362 | SCV005887011 | benign | not specified | 2025-01-27 | criteria provided, single submitter | clinical testing | Variant summary: KCND2 c.670C>A alters a conserved nucleotide resulting in a synonymous change. Several computational tools predict a significant impact on normal splicing: Four predict the variant abolishes a cryptic 5' donor site. However, these predictions have yet to be confirmed by functional studies. The variant allele was found at a frequency of 0.0014 in 251430 control chromosomes in the gnomAD database, including 6 homozygotes. The observed variant frequency is approximately 221 fold of the estimated maximal expected allele frequency for a pathogenic variant in KCND2 causing Arrhythmia phenotype (6.3e-06). To our knowledge, no occurrence of c.670C>A in individuals affected with Arrhythmia and no experimental evidence demonstrating its impact on protein function have been reported. ClinVar contains an entry for this variant (Variation ID: 529732). Based on the evidence outlined above, the variant was classified as benign. |