Total submissions: 7
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000255332 | SCV000321387 | pathogenic | not provided | 2021-12-09 | criteria provided, single submitter | clinical testing | Nonsense 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: 25525159, 15241804, 28025403, 32180488) |
Eurofins Ntd Llc |
RCV000255332 | SCV000339070 | pathogenic | not provided | 2016-02-17 | criteria provided, single submitter | clinical testing | |
Illumina Laboratory Services, |
RCV000316840 | SCV000401252 | likely pathogenic | Sjögren-Larsson syndrome | 2017-05-04 | criteria provided, single submitter | clinical testing | The ALDH3A2 c.529C>T (p.Arg177Ter) variant is a stop-gained variant that has been reported in a compound heterozygous state with a second truncating variant in two unrelated individuals with Sjogren-Larsson syndrome (SLS), and in a heterozygous state in the unaffected father of one of the individuals (Carney et al. 2004; Nagappa et al. 2016). Control data are unavailable for the p.Arg177Ter variant, which is reported at a frequency of 0.00042 in the Latino population of the Genome Aggregation Database. FALDH activity in cultured skin fibroblasts from one of the individuals was 4% that of normal fibroblasts (Carney et al. 2004). Based on the evidence from the literature and the potential impact of stop-gained variants, the p.Arg177Ter variant is classified as likely pathogenic for Sjogren-Larsson syndrome. This variant was observed by ICSL as part of a predisposition screen in an ostensibly healthy population. |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV000316840 | SCV000918412 | pathogenic | Sjögren-Larsson syndrome | 2018-09-03 | criteria provided, single submitter | clinical testing | Variant summary: ALDH3A2 c.529C>T (p.Arg177X) 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. A truncation downstream of this position has been classified as pathogenic by our laboratory (eg. c.1291_1292delAA (p.Lys431fsX5)). The variant allele was found at a frequency of 5.7e-05 in 246266 control chromosomes (gnomAD). This frequency is not significantly higher than expected for a pathogenic variant in ALDH3A2 causing Sjogren-Larsson Syndrome (5.7e-05 vs 0.0018), allowing no conclusion about variant significance. c.529C>T has been reported in the literature in individuals affected with Sjogren-Larsson Syndrome, in one case the patient was reported to have <10% enzyme activity (Carney_2004, Nagappa_2017). Four ClinVar submissions from other clinical diagnostic laboratories (evaluation after 2014) cite the variant as pathogenic (3x) and once as uncertain significance. Based on the evidence outlined above, the variant was classified as pathogenic. |
Labcorp Genetics |
RCV000255332 | SCV001212449 | pathogenic | not provided | 2024-08-13 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg177*) in the ALDH3A2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ALDH3A2 are known to be pathogenic (PMID: 10577908, 10854114). This variant is present in population databases (rs72547561, gnomAD 0.04%). This premature translational stop signal has been observed in individual(s) with Sjögren-Larsson syndrome (PMID: 15241804). ClinVar contains an entry for this variant (Variation ID: 265027). For these reasons, this variant has been classified as Pathogenic. |
Counsyl | RCV000316840 | SCV000800797 | pathogenic | Sjögren-Larsson syndrome | 2017-12-04 | no assertion criteria provided | clinical testing | |
Natera, |
RCV000316840 | SCV001459270 | pathogenic | Sjögren-Larsson syndrome | 2020-09-16 | no assertion criteria provided | clinical testing |