Total submissions: 12
| Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
|---|---|---|---|---|---|---|---|---|
| Myriad Genetics, |
RCV002288645 | SCV004931182 | likely pathogenic | Li-Fraumeni syndrome 1 | 2024-02-21 | criteria provided, single submitter | clinical testing | This variant is considered likely pathogenic. This variant occurs within a consensus splice junction and is predicted to result in abnormal mRNA splicing of either an out-of-frame exon or an in-frame exon necessary for protein stability and/or normal function. |
| Genomic Medicine Center of Excellence, |
RCV003992194 | SCV004809791 | pathogenic | Adrenocortical carcinoma, hereditary | 2024-04-04 | criteria provided, single submitter | clinical testing | |
| Genome- |
RCV002288645 | SCV002583100 | pathogenic | Li-Fraumeni syndrome 1 | 2022-06-18 | criteria provided, single submitter | clinical testing | |
| Genome- |
RCV000131124 | SCV002582438 | pathogenic | Hereditary cancer-predisposing syndrome | 2022-06-18 | criteria provided, single submitter | clinical testing | |
| Gene |
RCV000786811 | SCV001816973 | pathogenic | not provided | 2019-12-13 | criteria provided, single submitter | clinical testing | Canonical splice site variant in a gene for which loss-of-function is a known mechanism of disease; Observed in individuals with history consistent with pathogenic variants in this gene referred for genetic testing at GeneDx and in published literature (Hwang 2003); Not observed in large population cohorts (Lek 2016); This variant is associated with the following publications: (PMID: 31105275, 30720243, 25045116, 25525159, 12610779, 24240112, 23374397) |
| Labcorp Genetics |
RCV001380070 | SCV001578012 | pathogenic | Li-Fraumeni syndrome | 2023-12-22 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 9 of the TP53 gene. RNA analysis indicates that disruption of this splice site induces altered splicing and may result in an absent or disrupted protein product. This variant is not present in population databases (gnomAD no frequency). Disruption of this splice site has been observed in individuals with clinical features of Li Fraumeni syndrome (PMID: 10980596, 12610779, 20522432, 26014290, 26911350). ClinVar contains an entry for this variant (Variation ID: 142161). Studies have shown that disruption of this splice site results in the inclusion of a portion of intron 9 and introduces a premature termination codon (PMID: 10980596). The resulting mRNA is expected to undergo nonsense-mediated decay. For these reasons, this variant has been classified as Pathogenic. |
| Ambry Genetics | RCV000131124 | SCV000186055 | pathogenic | Hereditary cancer-predisposing syndrome | 2018-10-25 | criteria provided, single submitter | clinical testing | The c.994-1G>A intronic pathogenic mutation results from a G to A substitution one nucleotide upstream from coding exon 9 of the TP53 gene This aleration was reported in an individual with classic Li-Fraumeni syndrome (Hwang SJ et al. Am J Hum Genet. 2003 Apr;72(4):975-83). In addition to the clinical data presented in the literature, alterations that disrupt the canonical splice site are expected to cause aberrant splicing, resulting in an abnormal protein or a transcript that is subject to nonsense-mediated mRNA decay. As such, this alteration is classified as a disease-causing mutation. |
| Dr. |
RCV005886927 | SCV006897647 | not provided | Ovarian serous cystadenocarcinoma | no classification provided | in vitro | ||
| Dr. |
RCV005886927 | SCV006897646 | not provided | Ovarian serous cystadenocarcinoma | no classification provided | in vitro | ||
| Dr. |
RCV005886926 | SCV006897644 | not provided | Colon adenocarcinoma | no classification provided | in vitro | ||
| Dr. |
RCV005886925 | SCV006897643 | not provided | Familial cancer of breast | no classification provided | in vitro | ||
| Mut |
RCV000786811 | SCV000925703 | not provided | not provided | no classification provided | in vitro |