Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Mendelics | RCV000989987 | SCV001140749 | likely pathogenic | Familial cancer of breast | 2019-05-28 | criteria provided, single submitter | clinical testing | |
Color Diagnostics, |
RCV001182221 | SCV001347580 | likely pathogenic | Hereditary cancer-predisposing syndrome | 2019-05-09 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001858716 | SCV002155466 | uncertain significance | Familial cancer of breast; Fanconi anemia complementation group J | 2023-12-01 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 19 of the BRIP1 gene. While this variant is not anticipated to result in nonsense mediated decay, it likely alters RNA splicing and results in a disrupted protein product. This variant is present in population databases (rs773639563, gnomAD 0.003%). Disruption of this splice site has been observed in individual(s) with thyroid carcinoma (PMID: 29625052). ClinVar contains an entry for this variant (Variation ID: 803448). Variants that disrupt the consensus splice site are a relatively common cause of aberrant splicing (PMID: 17576681, 9536098). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. In summary, the available evidence is currently insufficient to determine the role of this variant in disease. Therefore, it has been classified as a Variant of Uncertain Significance. |
Ambry Genetics | RCV001182221 | SCV005101026 | uncertain significance | Hereditary cancer-predisposing syndrome | 2024-04-18 | criteria provided, single submitter | clinical testing | The c.2906-1G>A intronic variant results from a G to A substitution one nucleotide upstream from coding exon 19 of the BRIP1 gene. In silico splice site analysis predicts that this alteration will weaken the native splice acceptor site and may result in the creation or strengthening of a novel splice acceptor site; however, direct evidence is insufficient at this time (Ambry internal data). The resulting transcript is predicted to be in-frame and is not expected to trigger nonsense-mediated mRNA decay; however, direct evidence is unavailable. The exact functional effect of the altered amino acid sequence is unknown. This nucleotide position is highly conserved in available vertebrate species. Based on the available evidence, the clinical significance of this variant remains unclear. |
Gene |
RCV004721693 | SCV005326577 | uncertain significance | not provided | 2024-01-23 | criteria provided, single submitter | clinical testing | Canonical splice site variant with an unclear effect on protein function; Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 29625052, 29922827, 36451132) |