Total submissions: 8
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Biesecker Lab/Clinical Genomics Section, |
RCV000171827 | SCV000054727 | uncertain significance | Hypertrophic cardiomyopathy | 2018-04-05 | criteria provided, single submitter | research | |
Laboratory for Molecular Medicine, |
RCV000036880 | SCV000060535 | uncertain significance | not specified | 2016-06-16 | criteria provided, single submitter | clinical testing | The p.Thr495Met variant in ACTN2 has been reported in at least 3 individuals wit h HCM, segregating with disease in 1 affected relative (Theis 2006, Chiu 2010). This variant has been previously identified by our laboratory in 3 individuals w ith HCM, one of which also carried a pathogenic variant in another gene. In addi tion, the p.Thr495Met variant in ACTN2 did not segregate with disease in two aff ected relatives from one family. This variant has also been identified in 22/651 34 European chromosomes by the Exome Aggregation Consortium (ExAC, http://exac.b roadinstitute.org; dbSNP rs200248944). Computational prediction tools and conser vation analysis suggest that this variant may impact the protein, though this in formation is not predictive enough to determine pathogenicity. In summary, due t o conflicting data, the clinical significance of the p.Thr495Met variant is unce rtain. |
Labcorp Genetics |
RCV000470355 | SCV000553751 | likely benign | Dilated cardiomyopathy 1AA; Primary familial hypertrophic cardiomyopathy | 2024-01-22 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001703876 | SCV000617053 | likely benign | not provided | 2021-04-07 | criteria provided, single submitter | clinical testing | This variant is associated with the following publications: (PMID: 23299917, 24082139, 20022194, 23861362, 26656175, 26312134, 28518168, 17097056, 32880476) |
CHEO Genetics Diagnostic Laboratory, |
RCV000769759 | SCV000901181 | uncertain significance | Cardiomyopathy | 2016-01-15 | criteria provided, single submitter | clinical testing | |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV000036880 | SCV002500165 | uncertain significance | not specified | 2022-03-07 | criteria provided, single submitter | clinical testing | Variant summary: ACTN2 c.1484C>T (p.Thr495Met) results in a non-conservative amino acid change in the encoded protein sequence. Three of five in-silico tools predict a damaging effect of the variant on protein function. The variant allele was found at a frequency of 0.00028 in 251310 control chromosomes in the gnomAD database, including 1 homozygote. The observed variant frequency is approximately 11 fold of the estimated maximal expected allele frequency for a pathogenic variant in ACTN2 causing Cardiomyopathy phenotype (2.5e-05), strongly suggesting that the variant is benign. c.1484C>T has been reported in the literature in an individual with Z-disk HCM within a cohort previously determined to be negative for mutations in the eight genes associated with myofilament-HCM (example, Theis_2006), in two individuals from a single family reportedly affected by HCM who were only screened for ACTN2 by high melt analysis (example, Chiu_2010), and as a VUS in settings of multigene panel testing in at-least two individuals among DCM cohorts (example, Akinrinade_2015, Verdonschot_2020). These report(s) do not provide unequivocal conclusions about association of the variant with Hypertrophic/Dilated Cardiomyopathy. To our knowledge, no experimental evidence demonstrating an impact on protein function has been reported. Five clinical diagnostic laboratories have submitted clinical-significance assessments for this variant to ClinVar after 2014 without evidence for independent evaluation (VUS, n=4; likely benign, n=1). Based on the evidence outlined above, the variant was classified as VUS-possibly benign. |
Ambry Genetics | RCV004018816 | SCV003702198 | uncertain significance | Cardiovascular phenotype | 2021-11-09 | criteria provided, single submitter | clinical testing | The c.1484C>T (p.T495M) alteration is located in exon 13 (coding exon 13) of the ACTN2 gene. This alteration results from a C to T substitution at nucleotide position 1484, causing the threonine (T) at amino acid position 495 to be replaced by a methionine (M). Based on insufficient or conflicting evidence, the clinical significance of this alteration remains unclear. |
OMIM | RCV000169901 | SCV000222235 | pathogenic | Cardiomyopathy, familial hypertrophic, 23, with or without ventricular noncompaction | 2010-03-16 | no assertion criteria provided | literature only |