Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000674003 | SCV000799272 | likely pathogenic | Alstrom syndrome | 2018-04-12 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002440414 | SCV002749019 | pathogenic | Cardiovascular phenotype | 2020-05-08 | criteria provided, single submitter | clinical testing | The c.2755dupT variant, located in coding exon 8 of the ALMS1 gene, results from a duplication of T at nucleotide position 2755, causing a translational frameshift with a predicted alternate stop codon (p.S919Ffs*12). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |
Labcorp Genetics |
RCV000674003 | SCV004380221 | pathogenic | Alstrom syndrome | 2022-12-17 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 557817). This variant has not been reported in the literature in individuals affected with ALMS1-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Ser919Phefs*12) in the ALMS1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ALMS1 are known to be pathogenic (PMID: 17594715). |