{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["46"],"submitter":["Rajaram S"],"pubmed_abstract":["New treatments are urgently required for triple-negative breast cancer (TNBC). As TP53 is mutated in approximately 80% of TNBC, it is theoretically an attractive target for new drugs for this disease. Arsenic trioxide (ATO), which is used to treat promyelocytic leukaemia, was recently shown to reactivate mutant p53 and restore wild-type functionality. The aim of this study was to evaluate ATO as a potential new treatment for TNBC. Using a panel of 20 cell lines, we found that TNBC cell lines were more sensitive to ATO than non-TNBC cell lines (P = 0.045). Consistent with its ability to reactivate mutant p53, ATO was a more potent inhibitor of proliferation in cell lines with mutant TP53 than the wildtype TP53 (P = 0.027). Direct evidence of mutant p53 reactivation was the induction of mult"],"journal":["Translational oncology"],"pagination":["102025"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11225897"],"repository":["biostudies-literature"],"pubmed_title":["Targeting mutant p53 with arsenic trioxide: A preclinical study focusing on triple negative breast cancer."],"pmcid":["PMC11225897"],"pubmed_authors":["Synnott NC","Rajaram S","Duffy MJ","Madden SF","Crown J"],"additional_accession":[]},"is_claimable":false,"name":"Targeting mutant p53 with arsenic trioxide: A preclinical study focusing on triple negative breast cancer.","description":"New treatments are urgently required for triple-negative breast cancer (TNBC). As TP53 is mutated in approximately 80% of TNBC, it is theoretically an attractive target for new drugs for this disease. Arsenic trioxide (ATO), which is used to treat promyelocytic leukaemia, was recently shown to reactivate mutant p53 and restore wild-type functionality. The aim of this study was to evaluate ATO as a potential new treatment for TNBC. Using a panel of 20 cell lines, we found that TNBC cell lines were more sensitive to ATO than non-TNBC cell lines (P = 0.045). Consistent with its ability to reactivate mutant p53, ATO was a more potent inhibitor of proliferation in cell lines with mutant TP53 than the wildtype TP53 (P = 0.027). Direct evidence of mutant p53 reactivation was the induction of mult","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2026-05-29T11:20:13.471Z","creation":"2025-04-04T12:54:15.198Z"},"accession":"S-EPMC11225897","cross_references":{"pubmed":["38870678"],"doi":["10.1016/j.tranon.2024.102025"]}}