Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Revvity Omics, |
RCV000779543 | SCV002025110 | likely pathogenic | Platelet-type bleeding disorder 10 | 2019-07-24 | criteria provided, single submitter | clinical testing | |
Gene |
RCV004722813 | SCV005332344 | likely pathogenic | not provided | 2023-06-29 | 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; Has not been previously published as pathogenic or benign to our knowledge; This variant is associated with the following publications: (PMID: 31589614) |
Division of Human Genetics, |
RCV000477879 | SCV000536864 | likely pathogenic | Platelet-type bleeding disorder 10; Coronary heart disease, susceptibility to, 7; Malaria, susceptibility to | 2016-03-26 | no assertion criteria provided | research | |
Prevention |
RCV004551576 | SCV004115600 | likely pathogenic | CD36-related disorder | 2024-03-23 | no assertion criteria provided | clinical testing | The CD36 c.1254+1G>A variant is predicted to disrupt the GT donor site and interfere with normal splicing. This variant was reported, heterozygous, in multiple individuals undergoing preconception carrier screening (Capalbo et al. 2019. PubMed ID: 31589614). It is unclear if any of these individuals were affected or if they carried additional variants in the CD36 gene. This variant is reported in 0.023% of alleles in individuals of European (Non-Finnish) descent in gnomAD. Variants that disrupt the consensus splice donor site in CD36 are expected to be pathogenic. This variant is interpreted as likely pathogenic. |