Total submissions: 13
| Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
|---|---|---|---|---|---|---|---|---|
| Center for Genomic Medicine, |
RCV006273840 | SCV007129820 | oncogenic | Neoplasm | 2025-12-29 | criteria provided, single submitter | clinical testing | |
| Myriad Genetics, |
RCV002289666 | SCV004932223 | 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. |
| Genome- |
RCV002289666 | SCV002583107 | pathogenic | Li-Fraumeni syndrome 1 | 2022-06-18 | criteria provided, single submitter | clinical testing | |
| Genome- |
RCV000492618 | SCV002582445 | pathogenic | Hereditary cancer-predisposing syndrome | 2022-06-18 | criteria provided, single submitter | clinical testing | |
| Labcorp Genetics |
RCV000808655 | SCV000948769 | pathogenic | Li-Fraumeni syndrome | 2021-08-28 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. ClinVar contains an entry for this variant (Variation ID: 428877). Disruption of this splice site has been observed in individual(s) with Li-Fraumeni syndrome (PMID: 29070607). In at least one individual the variant was observed to be de novo. This variant is not present in population databases (ExAC no frequency). This sequence change affects a donor splice site in intron 8 of the TP53 gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in TP53 are known to be pathogenic (PMID: 20522432). |
| Ambry Genetics | RCV000492618 | SCV000581110 | pathogenic | Hereditary cancer-predisposing syndrome | 2026-02-18 | criteria provided, single submitter | clinical testing | The c.919+2T>G intronic pathogenic mutation results from a T to G substitution 2 nucleotides after coding exon 7 in the TP53 gene. This pathogenic mutation has been detected as a de novo finding in an individual with metastatic early onset breast cancer (Ambry internal data). In silico splice site analysis predicts that this alteration will weaken the native splice donor site, and RNA evidence supports this prediction (Ambry internal data). Based on the supporting evidence, this variant is interpreted as a disease-causing mutation. |
| Dr. |
RCV005899764 | SCV006897716 | not provided | Malignant tumor of esophagus | no classification provided | in vitro | ||
| Dr. |
RCV005899764 | SCV006897715 | not provided | Malignant tumor of esophagus | no classification provided | in vitro | ||
| Dr. |
RCV005899765 | SCV006897714 | not provided | Ovarian serous cystadenocarcinoma | no classification provided | in vitro | ||
| Dr. |
RCV005899762 | SCV006897713 | not provided | Colon adenocarcinoma | no classification provided | in vitro | ||
| Dr. |
RCV005899763 | SCV006897712 | not provided | Squamous cell carcinoma of the head and neck | no classification provided | in vitro | ||
| Dr. |
RCV005899763 | SCV006897710 | not provided | Squamous cell carcinoma of the head and neck | no classification provided | in vitro | ||
| Mut |
RCV001542803 | SCV001761179 | not provided | not provided | no classification provided | in vivo |