Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
SIB Swiss Institute of Bioinformatics | RCV000505526 | SCV000787444 | likely pathogenic | Encephalopathy, neonatal severe, with lactic acidosis and brain abnormalities | 2018-04-16 | criteria provided, single submitter | curation | This variant is interpreted as a Likely Pathogenic, for Encephalopathy, neonatal severe, with lactic acidosis and brain abnormalities, Autosomal Recessive inheritance. The following ACMG Tag(s) were applied: PM2 => Absent from controls (or at extremely low frequency if recessive) in Exome Sequencing Project, 1000 Genomes Project, or Exome Aggregation Consortium. PS3 => Well-established functional studies show a deleterious effect (PMID:28757203). PM3 => For recessive disorders, detected in trans with a pathogenic variant (PMID:28757203). |
OMIM | RCV000505526 | SCV000599792 | pathogenic | Encephalopathy, neonatal severe, with lactic acidosis and brain abnormalities | 2017-09-15 | no assertion criteria provided | literature only | |
Prevention |
RCV004755942 | SCV005346629 | uncertain significance | LIPT2-related disorder | 2024-05-16 | no assertion criteria provided | clinical testing | The LIPT2 c.89T>C variant is predicted to result in the amino acid substitution p.Leu30Pro. This variant was reported together with second variant in an individual with severe neonatal encephalopathy and deleterious effect of this genotype was confirmed in patients fibroblasts (Habarou et al. 2017. PubMed ID: 28757203; Lebigot et al. 2017. PubMed ID: 28803783). This variant is reported in 0.011% of alleles in individuals of African descent in gnomAD. Although we suspect that this variant may be pathogenic, at this time, the clinical significance of this variant is uncertain due to the absence of conclusive functional and genetic evidence. |