Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001008594 | SCV001168367 | pathogenic | not provided | 2019-02-18 | criteria provided, single submitter | clinical testing | The c.225_226insTGCT variant in the IL2RG gene has not been reported previously as a pathogenic variant nor as a benign variant, to our knowledge. The c.225_226insTGCT variant causes a frameshift starting with codon Serine 76, changes this amino acid to a Cysteine residue, and creates a premature Stop codon at position 2 of the new reading frame, denoted p.Ser76CysfsX2. This variant is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. The c.225_226insTGCT variant is not observed in large population cohorts (Lek et al., 2016). We interpret c.225_226insTGCT as a pathogenic variant. |
Labcorp Genetics |
RCV001041771 | SCV001205408 | pathogenic | X-linked severe combined immunodeficiency | 2020-02-22 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in IL2RG are known to be pathogenic (PMID: 9058718, 10794430). This variant has not been reported in the literature in individuals with IL2RG-related conditions. This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Ser76Cysfs*2) in the IL2RG gene. It is expected to result in an absent or disrupted protein product. |