Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000685322 | SCV000812800 | pathogenic | Bethlem myopathy 1A | 2025-01-20 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg468*) in the COL6A2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in COL6A2 are known to be pathogenic (PMID: 19884007, 20976770). This variant is present in population databases (rs374669775, gnomAD 0.01%). This premature translational stop signal has been observed in individual(s) with autosomal recessive collagenopathy (PMID: 23326386, 29419890). ClinVar contains an entry for this variant (Variation ID: 565700). For these reasons, this variant has been classified as Pathogenic. |
Ce |
RCV001311585 | SCV001501819 | pathogenic | not provided | 2020-07-01 | criteria provided, single submitter | clinical testing | |
Genomic Medicine Center of Excellence, |
RCV003989581 | SCV004806453 | uncertain significance | Ullrich congenital muscular dystrophy 1B | 2024-03-25 | criteria provided, single submitter | clinical testing | |
Neurogenomics Lab, |
RCV005091997 | SCV005849065 | pathogenic | Collagen 6-related myopathy | 2025-02-10 | criteria provided, single submitter | research | PM2_supporting: the highest population allele frequency in gnomAD v2.1.1 is 0.0001001 (0.01%; 1/9990 alleles in Ashkenazi Jewish population) and the variant is absent from gnomAD v3.1.2 (adequate coverage >20X confirmed). The variant is absent from an internal database. PM1 met: this variant is in the collagen triple helix (TH) repeat domain together with other pathogenic variants (PMID 24038877). PS4_moderate: variant identified in at least 5 unrelated probands with consistent phenotype for disorder (PMID 23326386, 20976770, 37569848, 29419890). PVS1 met: null variant (nonsense, predicted to undergo NMD, exon is present in a biologically-relevant transcript in a gene where LOF is a known mechanism of disease). Sequencing funded by the International Centre for Genomic Medicine in Neuromuscular Diseases (ICGNMD): https://www.ucl.ac.uk/genomic-medicine-neuromuscular-diseases/. |
Gene |
RCV000685322 | SCV001519045 | not provided | Bethlem myopathy 1A | no assertion provided | literature only | Common variant that in homozygosity results in loss of function |