Total submissions: 7
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Laboratory for Molecular Medicine, |
RCV000036047 | SCV000059699 | pathogenic | Rare genetic deafness | 2017-09-12 | criteria provided, single submitter | clinical testing | The c.1344-2A>G variant in MYO7A has been reported in four individuals with Ushe r syndrome (Maubaret 2005, LMM data). One of them was homozygous for the variant and three other individuals were compound heterozygous with a second pathogenic MYO7A variant. This variant has not been identified in large population studies . In addition, this variant occurs in the invariant region (+/- 1/2) of the spli ce consensus sequence and is predicted to cause altered splicing leading to an a bnormal or absent protein. In summary, this variant meets criteria to be classif ied as pathogenic for Usher syndrome in an autosomal recessive manner. |
Counsyl | RCV000665311 | SCV000789408 | pathogenic | Autosomal recessive nonsyndromic hearing loss 2; Usher syndrome type 1 | 2017-02-08 | criteria provided, single submitter | clinical testing | |
Kariminejad - |
RCV001814023 | SCV001755202 | pathogenic | Ear malformation | 2021-07-10 | criteria provided, single submitter | clinical testing | |
INGEBI, |
RCV001544528 | SCV001763574 | pathogenic | Nonsyndromic genetic hearing loss | 2021-07-15 | criteria provided, single submitter | clinical testing | Based on ACMG/AMP guidelines and Hearing Loss Expert Panel specific criteria:The c.1344-2 A>G variant in MYO7A gene is absent from population databases meeting PM2. This type of variant is predicted to generate a lost of the aceptor splicing site in MYO7A gene affecting gene MYO7A, which is a known mechanism of disease, PVS1. The c.1344-2 A>G has been identified in trans with a pathogenic variant in an Ushers patient with altered balance (PMID:15823922). Besides, it was identified in homocygous state in two different families (one with severe-profound non-syndrmic hearing loss and the other with Usher Syndromce) and an sporadic case with Usher Syndrome; PMID: 26445815, 27460420.); PP4. In thi work, c.1344-2 A>G was detected in trans with a pathogenic variant in MYO7A gene in a child with non-syndormic hearing loss (ophtalmic features could appear in the youth); PM3_S. Taking into account all the information together: PM2, PVS1, PM3_S, PP4 the variant is classified as Pathogenics for non-syndromic hearing loss and Usher Syndrome. |
Labcorp Genetics |
RCV001852738 | SCV002236652 | pathogenic | not provided | 2023-11-25 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 12 of the MYO7A gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in MYO7A are known to be pathogenic (PMID: 8900236, 25404053). This variant is not present in population databases (gnomAD no frequency). Disruption of this splice site has been observed in individuals with autosomal recessive deafness and/or autosomal recessive Usher syndrome (PMID: 15823922, 26445815, 27460420). This variant is also known as c.1244-2A>G. ClinVar contains an entry for this variant (Variation ID: 43143). 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. |
Gene |
RCV001852738 | SCV002526468 | pathogenic | not provided | 2022-06-17 | criteria provided, single submitter | clinical testing | Canonical splice site variant predicted to result in a null allele 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: 15823922, 31479088) |
Natera, |
RCV001831626 | SCV002086575 | pathogenic | Usher syndrome type 1B | 2021-02-25 | no assertion criteria provided | clinical testing |