Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Center for Molecular Medicine, |
RCV001030042 | SCV001190563 | pathogenic | Carnitine acylcarnitine translocase deficiency | 2019-05-10 | criteria provided, single submitter | clinical testing | |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV001030042 | SCV001337811 | pathogenic | Carnitine acylcarnitine translocase deficiency | 2020-01-13 | criteria provided, single submitter | clinical testing | Variant summary: SLC25A20 c.270delC (p.Phe91LeufsX38) results in a premature termination codon, predicted to cause a truncation of the encoded protein or absence of the protein due to nonsense mediated decay, which are commonly known mechanisms for disease. Truncations downstream of this position have been classified as pathogenic by our laboratory. The variant was absent in 250358 control chromosomes. c.270delC has been reported in the literature in at-least one homozygous individual affected with Carnitine-Acylcarnitine Translocase Deficiency (Hsu_2001) and cited frequently by others (example, Wang_2011 and Costa_2003). These data indicate that the variant may be associated with disease. At least one publication reports experimental evidence evaluating an impact on protein function. The most pronounced variant effect results in <10% of normal CACT enzyme activity (Hsu_2001). No clinical diagnostic laboratories have submitted clinical-significance assessments for this variant to ClinVar after 2014. Based on the evidence outlined above, the variant was classified as pathogenic. |
Baylor Genetics | RCV001030042 | SCV004201728 | pathogenic | Carnitine acylcarnitine translocase deficiency | 2022-09-22 | criteria provided, single submitter | clinical testing |