Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000532364 | SCV000643045 | uncertain significance | Dilated cardiomyopathy 1G; Autosomal recessive limb-girdle muscular dystrophy type 2J | 2017-06-28 | criteria provided, single submitter | clinical testing | |
Broad Center for Mendelian Genomics, |
RCV001004945 | SCV001164469 | uncertain significance | Autosomal recessive limb-girdle muscular dystrophy type 2J | 2018-12-03 | criteria provided, single submitter | research | The heterozygous p.Thr11893Ser variant in TTN was identified by our study in the compound heterozygous state, with a likely pathogenic variant, in one individual with limb-girdle muscular dystrophy (LGMD). The presence of this variant in combination with a likely pathogenic variant and in an individual with LGMD increases the likelihood that the p.Thr11893Ser variant is pathogenic. This variant has been identified in 0.008833% (3/33964) of Latino chromosomes by the Genome Aggregation Database (gnomAD, http://gnomad.broadinstitute.org; dbSNP rs750832804). Although this variant has been seen in the general population, its frequency is low enough to be consistent with a recessive carrier frequency. Computational prediction tools and conservation analyses suggest that this variant may not impact the protein, though this information is not predictive enough to rule out pathogenicity. Additional computational tools suggest this variant may impact splicing, resulting in a frameshift and early termination codon. In summary, the clinical significance of p.Thr11893Ser variant is uncertain. ACMG/AMP Criteria applied: PM2, PM3_Supporting, BP4 (Richards 2015). |
Gene |
RCV001785656 | SCV002027931 | uncertain significance | not provided | 2023-02-06 | criteria provided, single submitter | clinical testing | Observed with a second TTN variant, phase unknown, in a patient with neonatal hypotonia in published literature (Gonzalez-Quereda et al., 2020); Not observed at a significant frequency in large population cohorts (gnomAD); Missense variant in a gene in which most reported pathogenic variants are truncating/loss-of-function; In silico analysis supports that this missense variant has a deleterious effect on protein structure/function; This variant is associated with the following publications: (PMID: 32403337) |