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Triple-negative breast cancer (TNBC) poses significant challenges in the field of oncology due to its prevalence and difficulty in treatment. TP53, which codes for a tumor-suppressing transcription factor p53, is crucial for the prevention of tumor development. When mutated, its role is reversed, as mutp53 provides new oncogenic properties and is correlated with the onset of cancers. Studies have presented a strong correlation between mutp53 and TNBC tumorigenesis by providing metastatic properties, uncontrolled proliferation, and immune evasion properties for the tumor cells. This review comprehensively examines the structural changes in mutp53, how the oncogenic properties are acquired through structural mutation, the cell signaling pathway that mutp53 alters that further leads to cancer development, and the novel treatments of TNBC using PRIMA-1, NVP-BEZ235, and histone deacetylase inhibitors (HDACIs). At last, the advantages of the treatments and challenges they currently are facing are critically evaluated. Further research directions, including examining toxicity and personalized treatments, are proposed for improving clinical outcomes for TNBC patients.
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Yucheng Bi (2025) studied this question.
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