Total submissions: 9
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Laboratory for Molecular Medicine, |
RCV000036431 | SCV000060086 | uncertain significance | not specified | 2010-02-03 | criteria provided, single submitter | clinical testing | |
Counsyl | RCV000670464 | SCV000795318 | uncertain significance | Pendred syndrome | 2017-11-14 | criteria provided, single submitter | clinical testing | |
Genome- |
RCV001785457 | SCV002027008 | uncertain significance | Autosomal recessive nonsyndromic hearing loss 4 | 2021-09-05 | criteria provided, single submitter | clinical testing | |
Genome- |
RCV000670464 | SCV002027009 | uncertain significance | Pendred syndrome | 2021-09-05 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV002490496 | SCV002804072 | uncertain significance | Autosomal recessive nonsyndromic hearing loss 4; Pendred syndrome | 2022-01-04 | criteria provided, single submitter | clinical testing | |
Revvity Omics, |
RCV003137559 | SCV003825644 | uncertain significance | not provided | 2022-05-30 | criteria provided, single submitter | clinical testing | |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV000036431 | SCV005381318 | uncertain significance | not specified | 2024-08-06 | criteria provided, single submitter | clinical testing | Variant summary: SLC26A4 c.1234G>A (p.Val412Ile) results in a conservative amino acid change located in the SLC26A/SulP transporter domain (IPR011547) of the encoded protein sequence. Three of five in-silico tools predict a benign effect of the variant on protein function. The variant allele was found at a frequency of 5.2e-05 in 250822 control chromosomes. This frequency is not significantly higher than estimated for a pathogenic variant in SLC26A4 causing Pendred Syndrome (5.2e-05 vs 0.0035), allowing no conclusion about variant significance. c.1234G>A has been reported in the literature in the heterozygous state, with no second variant identified, in individuals affected with Pendred Syndrome/Enlarged Vestibular Aqueduct (e.g. Landa_2013, Pang_2015, May_2019). These reports do not provide unequivocal conclusions about association of the variant with Pendred Syndrome. At least one publication reports experimental evidence evaluating an impact on protein function and found the variant has approximately 60% HCO3-/Cl- antiporter activity compared to the WT protein and was considered WT-like (Takahashi_2024). The following publications have been ascertained in the context of this evaluation (PMID: 23965030, 31633822, 26549381, 38474007). ClinVar contains an entry for this variant (Variation ID: 43499). Based on the evidence outlined above, the variant was classified as uncertain significance. |
Gene |
RCV003137559 | SCV005626492 | uncertain significance | not provided | 2024-07-12 | criteria provided, single submitter | clinical testing | In silico analysis indicates that this missense variant does not alter protein structure/function; Identified as a single heterozygous variant in a patient belonging to a cohort with hearing impairment and either goitre or EVA in published literature (PMID: 23965030); This variant is associated with the following publications: (PMID: 38474007, 27884173, 26549381, 30245029, 23965030) |
Natera, |
RCV000670464 | SCV001459868 | uncertain significance | Pendred syndrome | 2020-01-08 | no assertion criteria provided | clinical testing |