Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001390495 | SCV001592235 | pathogenic | Familial cancer of breast | 2024-04-22 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Lys862Argfs*9) in the PALB2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in PALB2 are known to be pathogenic (PMID: 17200668, 17200671, 17200672, 24136930, 25099575). This variant is present in population databases (rs752513498, gnomAD 0.003%). This variant has not been reported in the literature in individuals affected with PALB2-related conditions. ClinVar contains an entry for this variant (Variation ID: 1076548). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV001775034 | SCV002011814 | likely pathogenic | Hereditary cancer-predisposing syndrome | 2018-10-10 | criteria provided, single submitter | clinical testing | This variant results in an amino acid alteration, replacing a lysine (K) with an arginine (R) at position 862, creating a premature stop signal in the new reading frame (p.K862Rfs*9). The substitution is predicted to result in a non-functional PALB2 protein, either through protein truncation or nonsense-mediated mRNA decay. This variant is present in the gnomAD exomes database at a frequency of 0.00000398. Based on these findings and the limited literature regarding this substitution we consider it as a “likely pathogenic variant”. |
Ambry Genetics | RCV001775034 | SCV004007909 | pathogenic | Hereditary cancer-predisposing syndrome | 2023-05-01 | criteria provided, single submitter | clinical testing | The c.2585delA pathogenic mutation, located in coding exon 6 of the PALB2 gene, results from a deletion of one nucleotide at nucleotide position 2585, causing a translational frameshift with a predicted alternate stop codon (p.K862Rfs*9). One study detected this mutation in 0/3030 pancreatic cancer cases and 1/123136 population controls (Hu C et al. JAMA, 2018 Jun;319:2401-2409). In addition to the clinical data presented in the literature, 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. |
Myriad Genetics, |
RCV001390495 | SCV004188493 | pathogenic | Familial cancer of breast | 2023-09-13 | criteria provided, single submitter | clinical testing | This variant is considered pathogenic. This variant creates a frameshift predicted to result in premature protein truncation. |