Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000494064 | SCV000582138 | pathogenic | not provided | 2024-06-06 | criteria provided, single submitter | clinical testing | Frameshift variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; This variant is associated with the following publications: (PMID: 31589614, 11159947, 12429595) |
Fulgent Genetics, |
RCV001782989 | SCV002797358 | pathogenic | Glucocorticoid deficiency with achalasia | 2022-05-13 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000494064 | SCV003440540 | pathogenic | not provided | 2024-02-05 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Glu398Argfs*28) in the AAAS gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in AAAS are known to be pathogenic (PMID: 11159947). This variant is present in population databases (rs746305979, gnomAD 0.02%). This premature translational stop signal has been observed in individual(s) with achalasia-addisonianism-alacrimia syndrome (PMID: 12429595). This variant is also known as 1273 Ins A. ClinVar contains an entry for this variant (Variation ID: 429542). For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV003962360 | SCV004785665 | pathogenic | AAAS-related disorder | 2023-12-20 | no assertion criteria provided | clinical testing | The AAAS c.1191dupA variant is predicted to result in a frameshift and premature protein termination (p.Glu398Argfs*28). This variant was reported in the compound heterozygous state with a known causative AAAS variant in an individual with Triple-A syndrome (described as 1273 Ins A in Family 2, Houlden et al. 2002. PubMed ID: 12429595). This variant is reported in 0.020% of alleles in individuals of Latino descent in gnomAD. Frameshift variants in AAAS are expected to be pathogenic. This variant is interpreted as pathogenic. |