Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000954218 | SCV001100837 | benign | not provided | 2019-12-23 | criteria provided, single submitter | clinical testing | |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV001192861 | SCV001361284 | benign | not specified | 2019-11-06 | criteria provided, single submitter | clinical testing | Variant summary: APOA2 c.53-7_53-6dupTG alters a nucleotide located close to a canonical splice site and therefore could affect mRNA splicing, leading to a significantly altered protein sequence. 5/5 computational tools predict no significant impact on normal splicing. However, these predictions have yet to be confirmed by functional studies. The variant allele was found at a frequency of 0.036 in 28768 control chromosomes in the gnomAD database, including 28 homozygotes. The observed variant frequency is approximately 1823-folds over the estimated maximal expected allele frequency for a pathogenic variant in APOA2 causing Early Onset Coronary Artery Disease phenotype (2e-05), strongly suggesting that the variant is benign. Co-occurrences with other pathogenic variant(s) have been reported (LDLR c.1567G>A, p.Val523Met). No clinical diagnostic laboratories have submitted clinical-significance assessments for this variant to ClinVar after 2014. Based on the evidence outlined above, the variant was classified as benign. |
Diagnostic Laboratory, |
RCV000954218 | SCV001740753 | likely benign | not provided | no assertion criteria provided | clinical testing | ||
Genome Diagnostics Laboratory, |
RCV000954218 | SCV001927823 | likely benign | not provided | no assertion criteria provided | clinical testing | ||
Clinical Genetics DNA and cytogenetics Diagnostics Lab, |
RCV001192861 | SCV001971664 | benign | not specified | no assertion criteria provided | clinical testing |