Total submissions: 6
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000668682 | SCV000793323 | likely pathogenic | Merosin deficient congenital muscular dystrophy | 2017-08-10 | criteria provided, single submitter | clinical testing | |
Department Of Genetics, |
RCV000668682 | SCV000891602 | pathogenic | Merosin deficient congenital muscular dystrophy | 2017-12-30 | criteria provided, single submitter | curation | |
Illumina Laboratory Services, |
RCV000779487 | SCV000916120 | likely pathogenic | Congenital muscular dystrophy due to partial LAMA2 deficiency | 2024-09-05 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000824022 | SCV000964897 | pathogenic | LAMA2-related muscular dystrophy | 2023-11-11 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg2630*) 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). This variant is present in population databases (rs727502851, gnomAD 0.004%). This premature translational stop signal has been observed in individual(s) with clinical features of LAMA2-related conditions (PMID: 21520333). ClinVar contains an entry for this variant (Variation ID: 162579). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Revvity Omics, |
RCV001781490 | SCV002016436 | pathogenic | not provided | 2020-10-21 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV000668682 | SCV005059891 | pathogenic | Merosin deficient congenital muscular dystrophy | 2024-02-05 | criteria provided, single submitter | clinical testing |