Total submissions: 7
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Mendelics | RCV000987420 | SCV001136710 | pathogenic | Retinitis pigmentosa 41 | 2019-05-28 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001049161 | SCV001213195 | pathogenic | not provided | 2025-01-06 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 17 of the PROM1 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 PROM1 are known to be pathogenic (PMID: 17605048, 19718270, 24154662, 25474345). The frequency data for this variant in the population databases is considered unreliable, as metrics indicate poor data quality at this position in the gnomAD database. Disruption of this splice site has been observed in individuals with autosomal recessive PROM1-related retinal dystrophy (PMID: 24516651, 31129250). ClinVar contains an entry for this variant (Variation ID: 802053). 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. |
DBGen Ocular Genomics | RCV000987420 | SCV001815932 | pathogenic | Retinitis pigmentosa 41 | 2021-06-21 | criteria provided, single submitter | clinical testing | |
Ophthalmic Genetics Group, |
RCV003324540 | SCV004030438 | pathogenic | Cone-rod dystrophy | 2023-07-24 | criteria provided, single submitter | research | Clinical significance based on ACMG v2.0 |
Ophthalmic Genetics Group, |
RCV003324541 | SCV004030439 | pathogenic | Leber congenital amaurosis | 2023-07-24 | criteria provided, single submitter | research | Clinical significance based on ACMG v2.0 |
Prevention |
RCV004536013 | SCV004113255 | pathogenic | PROM1-related disorder | 2023-08-08 | criteria provided, single submitter | clinical testing | The PROM1 c.1984-1G>T variant is predicted to disrupt the AG splice acceptor site and interfere with normal splicing. This variant been reported in multiple individuals with autosomal recessive retinitis pigmentosa (de Castro-Miró et al 2014. PubMed ID: 24516651) and autosomal recessive cone-rod dystrophy (Del Pozo-Valero M et al 2019. PubMed ID: 31129250). This variant is reported in 0.0095% of alleles in individuals of Latino descent in gnomAD (http://gnomad.broadinstitute.org/variant/4-15991448-C-A). Variants that disrupt the consensus splice acceptor site in PROM1 are expected to be pathogenic. This variant is interpreted as pathogenic. |
Ophthalmo- |
RCV002467454 | SCV002762718 | pathogenic | Stargardt disease | 2022-12-14 | no assertion criteria provided | research |