Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000483565 | SCV000567678 | pathogenic | not provided | 2015-08-14 | criteria provided, single submitter | clinical testing | The c.2760_2763delTAAG deletion in the NSD1 gene has been reported previously in association with Sotos syndrome (Saugier-Veber et al., 2007; Rio et al., 2003). The deletion causes a frameshift starting with codon Serine 920, changes this amino acid to a Arginine residue and creates a premature Stop codon at position 7 of the new reading frame, denoted p.Ser920ArgfsX7. This variant is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. Therefore, we interpret c.2760_2763delTAAG as a pathogenic variant. |
Labcorp Genetics |
RCV001221224 | SCV001393252 | pathogenic | Beckwith-Wiedemann syndrome | 2019-05-04 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Ser920Argfs*7) in the NSD1 gene. It is expected to result in an absent or disrupted protein product. This variant is not present in population databases (ExAC no frequency). This variant has been observed to be de novo in individuals affected with Sotos syndrome (PMID: 12807965, 17565729). ClinVar contains an entry for this variant (Variation ID: 419698). Loss-of-function variants in NSD1 are known to be pathogenic (PMID: 12464997, 14571271, 15942875, 16247291). For these reasons, this variant has been classified as Pathogenic. |
Genome- |
RCV003231503 | SCV002054919 | pathogenic | Sotos syndrome | 2021-07-15 | criteria provided, single submitter | clinical testing |