{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T21:09:44Z","timestamp":1793740184525,"version":"4.6.1"},"reference-count":179,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,6]],"date-time":"2026-02-06T00:00:00Z","timestamp":1770336000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Mutant p53(Mtp53) not only loses its canonical tumor-suppressive functions but also acquires oncogenic gain-of-function properties, positioning it as a central orchestrator in reshaping the tumor immune microenvironment. This review systematically delineates how Mtp53 actively establishes and sustains an immunosuppressive niche through multiple interconnected mechanisms, including chronic inflammation, immune cell dysfunction, reprogramming of cancer-associated fibroblasts, metabolic dysregulation, epigenetic hijacking, and potentially aberrant liquid\u2013liquid phase separation, thereby promoting immune evasion and therapeutic resistance. We integrate current evidence to propose a conceptual \u201cmetabolism\u2013epigenetics\u2013immunity\u201d axis: Mtp53-driven metabolic reprogramming\u2014such as accumulation of lactate or \u03b1-ketoglutarate\u2014can modulate chromatin modifications and immune gene expression. Notably, the full\n                    <jats:italic>in vivo<\/jats:italic>\n                    causal chain of this axis remains unestablished; existing support derives primarily from stepwise experimental data and strong correlations. The immunological impact of Mtp53 is highly context-dependent, shaped by co-mutations and tissue origin. In TP53\/KRAS co-mutant non-small cell lung cancer (NSCLC), Mtp53 enhances tumor immunogenicity and improves response to\u00a0immune checkpoint inhibitors (ICIs); conversely, in immunologically \u201ccold\u201d\u00a0tumors\u2014such as triple-negative breast cancer, pancreatic ductal adenocarcinoma, and colorectal cancer\u2014it promotes T-cell exhaustion or myeloid suppression, reflecting marked cancer-type heterogeneity. Therapeutic approaches include Mtp53 reactivators (e.g., APR-246, PC14586), degraders, synthetic lethal strategies, and neoantigen vaccines. Although APR-246 showed efficacy in a phase II trial (NCT03072043), it failed to improve survival in phase III (NCT03745716) due to lack of TP53 mutation stratification. Its combination with pembrolizumab (NCT04383938) demonstrated acceptable safety (immune-related adverse events in \u223c12%) but limited efficacy, underscoring the need for biomarker-guided, precision-based combinations. Thus, a multidimensional biomarker platform is urgently needed\u2014one integrating TP53 mutation subtypes (e.g., R175H\n                    <jats:italic>vs<\/jats:italic>\n                    . nonsense mutations), dynamic ctDNA monitoring (VAF \u2265 0.01%), tumor immune microenvironment (TIME) features (e.g., TILs, MDSCs), and spatial multi-omics\u2014to enable precise molecular stratification and personalized intervention in Mtp53-driven cancers.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1753215","type":"journal-article","created":{"date-parts":[[2026,2,6]],"date-time":"2026-02-06T06:36:14Z","timestamp":1770359774000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":17,"title":["The impact of p53 mutation on tumor immune evasion: mechanistic insights and clinical implications"],"prefix":"10.3389","volume":"17","author":[{"given":"Luo","family":"Liang","sequence":"first","affiliation":[{"name":"Department of Radiation Oncology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China","place":["Chengdu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weidong","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Head and Neck Radiation Oncology, Radiation Oncology Key Laboratory of Sichuan Province, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China","place":["Chengdu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,2,6]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/278261a0","article-title":"T antigen is bound to a host protein in SV40-transformed 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