Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001086604 | SCV000541879 | likely benign | Neuroblastoma, susceptibility to, 3 | 2024-01-11 | criteria provided, single submitter | clinical testing | |
Gene |
RCV000657739 | SCV000779490 | uncertain significance | not provided | 2024-07-18 | 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 not an established mechanism of disease; Observed in a patient with intraductal papillary mucinous neoplasm (PMID: 30716324); This variant is associated with the following publications: (PMID: 30716324) |
Ambry Genetics | RCV001021020 | SCV001182582 | uncertain significance | Hereditary cancer-predisposing syndrome | 2022-11-30 | criteria provided, single submitter | clinical testing | The p.R1248* variant (also known as c.3742C>T), located in coding exon 24 of the ALK gene, results from a C to T substitution at nucleotide position 3742. This changes the amino acid from an arginine to a stop codon within coding exon 24. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. However, loss of function in ALK has not been clearly established as a mechanism of disease. Since supporting evidence is limited at this time, the clinical significance of this alteration remains unclear. |
Sema4, |
RCV001021020 | SCV002528490 | likely benign | Hereditary cancer-predisposing syndrome | 2020-07-21 | criteria provided, single submitter | curation |