Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001060563 | SCV001225262 | pathogenic | Aspartylglucosaminuria | 2019-11-17 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in AGA are known to be pathogenic (PMID: 7627186, 11309371). This variant has been observed in an individual affected with aspartylglucosaminuria (PMID: 8457202). This variant is also known as a 5 bp deletion (ACACA) in the literature. This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Thr123Hisfs*20) in the AGA gene. It is expected to result in an absent or disrupted protein product. |
Genomic Medicine Lab, |
RCV001060563 | SCV001573055 | pathogenic | Aspartylglucosaminuria | 2019-12-05 | criteria provided, single submitter | clinical testing | |
Myriad Genetics, |
RCV001060563 | SCV002060047 | likely pathogenic | Aspartylglucosaminuria | 2021-11-16 | criteria provided, single submitter | clinical testing | NM_000027.3(AGA):c.367_371del5(T123Hfs*20) is a frameshifting truncation variant classified as likely pathogenic in the context of aspartylglucosaminuria. T123Hfs*20 has not been observed in cases with relevant disease. Functional assessments of this variant are not available in the literature. T123Hfs*20 has not been observed in population frequency databases. In summary, NM_000027.3(AGA):c.367_371del5(T123Hfs*20) is a frameshifting truncation variant in a gene where loss of function is a known mechanism of disease and is predicted to disrupt protein function. Please note: this variant was assessed in the context of healthy population screening. |
Baylor Genetics | RCV001060563 | SCV004217582 | pathogenic | Aspartylglucosaminuria | 2023-09-29 | criteria provided, single submitter | clinical testing |