Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Center of Genomic medicine, |
RCV000503601 | SCV000598150 | likely pathogenic | Congenital myopathy with fiber type disproportion | 2016-09-26 | criteria provided, single submitter | clinical testing | |
Eurofins Ntd Llc |
RCV000727596 | SCV000854845 | uncertain significance | not provided | 2018-07-17 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000806717 | SCV000946731 | likely pathogenic | Congenital myopathy 4B, autosomal recessive; Congenital myopathy with fiber type disproportion | 2019-01-07 | criteria provided, single submitter | clinical testing | This sequence change replaces aspartic acid with histidine at codon 15 of the TPM3 protein (p.Asp15His). The aspartic acid residue is highly conserved and there is a moderate physicochemical difference between aspartic acid and histidine. This variant is not present in population databases (ExAC no frequency). This variant has been observed to be de novo in an individual affected with congenital hypotonia and muscle weakness (Invitae). ClinVar contains an entry for this variant (Variation ID: 437430). Algorithms developed to predict the effect of missense changes on protein structure and function (SIFT, PolyPhen-2, Align-GVGD) all suggest that this variant is likely to be disruptive, but these predictions have not been confirmed by published functional studies and their clinical significance is uncertain. In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. |