Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000670228 | SCV000795058 | likely pathogenic | Bloom syndrome | 2017-10-25 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000670228 | SCV001411379 | pathogenic | Bloom syndrome | 2019-08-18 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Pro1297Glnfs*3) in the BLM gene. It is expected to result in an absent or disrupted protein product. This variant is not present in population databases (ExAC no frequency). For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in BLM are known to be pathogenic (PMID: 17407155). This variant has not been reported in the literature in individuals with BLM-related conditions. ClinVar contains an entry for this variant (Variation ID: 554568). |
Ambry Genetics | RCV002352094 | SCV002620647 | pathogenic | Hereditary cancer-predisposing syndrome | 2020-11-02 | criteria provided, single submitter | clinical testing | The c.3890delC variant, located in coding exon 20 of the BLM gene, results from a deletion of one nucleotide at nucleotide position 3890, causing a translational frameshift with a predicted alternate stop codon (p.P1297Qfs*3). 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. |