<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>46</volume><submitter>Rajaram S</submitter><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</pubmed_abstract><journal>Translational oncology</journal><pagination>102025</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11225897</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Targeting mutant p53 with arsenic trioxide: A preclinical study focusing on triple negative breast cancer.</pubmed_title><pmcid>PMC11225897</pmcid><pubmed_authors>Synnott NC</pubmed_authors><pubmed_authors>Rajaram S</pubmed_authors><pubmed_authors>Duffy MJ</pubmed_authors><pubmed_authors>Madden SF</pubmed_authors><pubmed_authors>Crown J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Targeting mutant p53 with arsenic trioxide: A preclinical study focusing on triple negative breast cancer.</name><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</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Aug</publication><modification>2026-05-29T11:20:13.471Z</modification><creation>2025-04-04T12:54:15.198Z</creation></dates><accession>S-EPMC11225897</accession><cross_references><pubmed>38870678</pubmed><doi>10.1016/j.tranon.2024.102025</doi></cross_references></HashMap>