Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000674609 | SCV000799975 | pathogenic | Merosin deficient congenital muscular dystrophy | 2018-05-15 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV002499190 | SCV002806895 | likely pathogenic | Merosin deficient congenital muscular dystrophy; Muscular dystrophy, limb-girdle, autosomal recessive 23 | 2022-05-11 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV002531357 | SCV003440017 | pathogenic | LAMA2-related muscular dystrophy | 2023-01-17 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 558356). This premature translational stop signal has been observed in individual(s) with congenital muscular dystrophy (PMID: 18700894, 25124546). This variant is present in population databases (no rsID available, gnomAD 0.007%). This sequence change creates a premature translational stop signal (p.Asp2498Glufs*4) in the LAMA2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in LAMA2 are known to be pathogenic (PMID: 18700894, 32904964). |
Gene |
RCV003126901 | SCV003803388 | pathogenic | not provided | 2022-08-10 | criteria provided, single submitter | clinical testing | Observed with a second LAMA2 variant in a patient with congenital muscular dystrophy in the literature (Oliveira et al., 2008); Frameshift variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 18700894, 25124546) |