Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000664968 | SCV000789014 | likely pathogenic | Neuronal ceroid lipofuscinosis 3 | 2016-12-27 | criteria provided, single submitter | clinical testing | |
Invitae | RCV001868197 | SCV002234992 | pathogenic | Neuronal ceroid lipofuscinosis | 2023-12-19 | criteria provided, single submitter | clinical testing | This sequence change affects the initiator methionine of the CLN3 mRNA. The next in-frame methionine is located at codon 55. This variant is present in population databases (rs386833708, gnomAD 0.006%). Disruption of the initiator codon has been observed in individuals with Neuronal ceroid lipofuscinosis and/or retinitis pigmentosa (PMID: 32154056; Invitae). ClinVar contains an entry for this variant (Variation ID: 550268). For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV003420170 | SCV004107270 | likely pathogenic | CLN3-related disorder | 2023-04-28 | criteria provided, single submitter | clinical testing | The CLN3 c.1A>G variant is predicted to disrupt the translation initiation site (Start loss). This variant has not been reported in the literature, however other variant c.1A>C disrupting initiation codon has been reported in compound heterozygous state in three individuals with attenuated form of CLN3 disease (Kuper et al 2020. PubMed ID: 32154056). This variant is reported in 0.0058% of alleles in individuals of Latino descent in gnomAD (http://gnomad.broadinstitute.org/variant/16-28503080-T-C). In summary, we interpret this variant as likely pathogenic. |