Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Clin |
RCV001507045 | SCV001711996 | likely pathogenic | Pitt-Hopkins syndrome | 2021-03-26 | reviewed by expert panel | curation | The p.Leu609Pro variant in TCF4 occurs in the de novo state (biological parentage confirmed) in an affected individual (PS2). The p.Leu609Pro variant occurs in the well-characterized basic Helix-Loop-Helix domain (bHLH) functional domain of TCF4 (PM1). The p.Leu609Pro variant in TCF4 is absent from gnomAD (PM2_Supporting). Computational prediction analysis tools suggests a deleterious impact; however, this information does not predict clinical significance on its own (PP3). In summary, the p.Leu609Pro variant in TCF4 is classified as likely pathogenic for Pitt-Hopkins syndrome based on the ACMG/AMP criteria (PS2, PM1, PM2_supporting, PP3). |
Gene |
RCV000418798 | SCV000536543 | likely pathogenic | not provided | 2017-02-06 | criteria provided, single submitter | clinical testing | The L609P variant in the TCF4 gene has not been reported previously as a pathogenic variant, nor as a benign variant, to our knowledge. The L609P variant is not observed in large population cohorts (Lek et al., 2016; 1000 Genomes Consortium et al., 2015; Exome Variant Server). The L609P variant is a semi-conservative amino acid substitution, which may impact secondary protein structure as these residues differ in some properties. This substitution occurs at a position [that is conserved across species. In silico analysis predicts this variant is probably damaging to the protein structure/function. The L609P variant is a strong candidate for a pathogenic variant. |