ClinVar Miner

Submissions for variant NM_000546.6(TP53):c.722C>G (p.Ser241Cys)

dbSNP: rs28934573
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Total submissions: 10
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Submitter RCV SCV Clinical significance Condition Last evaluated Review status Method Comment
Dasa RCV000236210 SCV007599480 pathogenic not provided 2024-06-13 criteria provided, single submitter clinical testing NM_000546.6(TP53):c.722C>G (p.Ser241Cys) is a missense variant that results in the substitution of serine with cysteine. The affected residue or protein region has prior evidence supporting clinical relevance. This variant has been reported in individuals with related phenotype. Functional evidence supports a deleterious effect on the gene or gene product. The variant is present at low frequency in population datasets. Based on the available data, this variant is classified as pathogenic.
Center for Genomic Medicine, Rigshospitalet, Copenhagen University Hospital RCV006273569 SCV007129856 likely oncogenic Neoplasm 2025-12-29 criteria provided, single submitter clinical testing
Myriad Genetics, Inc. RCV002288664 SCV004932198 likely pathogenic Li-Fraumeni syndrome 1 2024-02-16 criteria provided, single submitter clinical testing This variant is considered likely pathogenic. Functional studies indicate this variant impacts protein function [PMID: 29979965]. This variant is expected to disrupt protein structure [Myriad internal data].
Labcorp Genetics (formerly Invitae), Labcorp RCV000154419 SCV003253335 likely pathogenic Li-Fraumeni syndrome 2024-06-09 criteria provided, single submitter clinical testing This sequence change replaces serine, which is neutral and polar, with cysteine, which is neutral and slightly polar, at codon 241 of the TP53 protein (p.Ser241Cys). This variant is not present in population databases (gnomAD no frequency). This missense change has been observed in individual(s) with Li-Fraumeni syndrome and/or ovarian cancer (PMID: 30730202, 35451682). ClinVar contains an entry for this variant (Variation ID: 177791). Advanced modeling performed at Invitae incorporating data from internal and/or published experimental studies (PMID: 12826609, 29979965, 30224644) indicates that this missense variant is expected to disrupt TP53 function with a positive predictive value of 97.5%. Experimental studies have shown that this missense change affects TP53 function (PMID: 12826609, 29979965, 30224644). In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic.
Genome-Nilou Lab RCV002288664 SCV002583024 likely pathogenic Li-Fraumeni syndrome 1 2022-06-18 criteria provided, single submitter clinical testing
Genome-Nilou Lab RCV000492778 SCV002582363 likely pathogenic Hereditary cancer-predisposing syndrome 2022-06-18 criteria provided, single submitter clinical testing
Ambry Genetics RCV000492778 SCV000581139 pathogenic Hereditary cancer-predisposing syndrome 2025-05-23 criteria provided, single submitter clinical testing The p.S241C pathogenic mutation (also known as c.722C>G), located in coding exon 6 of the TP53 gene, results from a C to G substitution at nucleotide position 722. The serine at codon 241 is replaced by cysteine, an amino acid with dissimilar properties. This variant is in the DNA binding domain of the TP53 protein and is reported to have non-functional transactivation in yeast-based assays (Kato S et al. Proc. Natl. Acad. Sci. USA. 2003 Jul;100:8424-9). Studies conducted in human cell lines indicate this alteration is deficient at growth suppression and has a dominant negative effect (Kotler E et al. Mol.Cell. 2018 Jul;71:178-190.e8; Giacomelli AO et al. Nat. Genet. 2018 Oct;50:1381-1387). This mutation has been identified in a family meeting classic Li-Fraumeni syndrome criteria (Sejben A et al. Orv Hetil 2019 Feb;160(6):228-234). This alteration has been observed numerous times as a somatic mutation in the cancerhotspots.org database (Chang MT et al. Cancer Discov. 2018 02;8:174-183). This variant was detected in at least one individual at an allele fraction that is suggestive of clonal hematopoiesis, a predictor of TP53 pathogenicity (Ambry internal data; Fortuno C et al. Genet Med. 2022 03;24:673-680). This amino acid position is highly conserved in available vertebrate species. This variant is considered to be rare based on population cohorts in the Genome Aggregation Database (gnomAD). In addition, this alteration is predicted to be deleterious by in silico analysis. Based on the supporting evidence, this alteration is interpreted as a disease-causing mutation.
GeneDx RCV000236210 SCV000293500 pathogenic not provided 2024-01-05 criteria provided, single submitter clinical testing Published functional studies demonstrate a damaging effect: non-functional transactivation and impaired growth suppression activity (PMID: 12826609, 29979965, 30224644, 20407015); Not observed at significant frequency in large population cohorts (gnomAD); In silico analysis supports that this missense variant has a deleterious effect on protein structure/function; This variant is associated with the following publications: (PMID: 20407015, 16312222, 24997986, 11301359, 23168708, 12144684, 15564288, 2024123, 8934544, 11079169, 11389059, 15064998, 16174251, 10690522, 21552959, 10951339, 15837541, 9792155, 25839328, 23349305, 15915369, 20404136, 19509155, 25356985, 28803919, 28861920, 30840781, 30224644, 29979965, 26619011, 34273903, 15510160, 35451682, 12826609, 30730202)
German Consortium for Hereditary Breast and Ovarian Cancer, University Hospital Cologne RCV000785321 SCV000923889 likely pathogenic Ovarian neoplasm 2018-12-01 no assertion criteria provided research
Laboratory for Molecular Medicine, Mass General Brigham Personalized Medicine RCV000154419 SCV000204087 likely pathogenic Li-Fraumeni syndrome 2008-01-03 no assertion criteria provided clinical testing

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