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Cancer"],"accepted":{"date-parts":[[2026,5,5]]},"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Urothelial carcinoma (UC) exhibits extensive infiltration of tumor-associated macrophages (TAMs). As the most frequently altered gene in UC,\n                      <jats:italic>TP53<\/jats:italic>\n                      is recognized not only as a guardian of genomic integrity, but also as a potential architect of the tumor immune microenvironment (TIME). However, how aberrant p53 status, comprising\n                      <jats:italic>TP53<\/jats:italic>\n                      mutation (\n                      <jats:italic>TP53<\/jats:italic>\n                      <jats:sup>Mut<\/jats:sup>\n                      ) and p53 abnormal expression (p53\n                      <jats:sup>Abn<\/jats:sup>\n                      ), correlates with TAM phenotypic and functional heterogeneity and their reciprocal interactions within the TIME landscape remains incompletely defined.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This study integrated single-cell RNA sequencing, immunohistochemistry, and flow cytometry to delineate TAM phenotypes and map distinct immune landscapes stratified by p53 status. Clinical relevance was assessed in a multicohort dataset of 962 patients with UC with comprehensive clinicopathological annotations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Single-cell profiling revealed distinct TAM subsets closely linked to p53 status. Interferon-primed TAMs, marked by\n                      <jats:italic>CXCL9<\/jats:italic>\n                      ,\n                      <jats:italic>CXCL10<\/jats:italic>\n                      ,\n                      <jats:italic>CXCL11<\/jats:italic>\n                      and\n                      <jats:italic>IDO1<\/jats:italic>\n                      , predominated in p53 wild-type (p53\n                      <jats:sup>WT<\/jats:sup>\n                      ) tumors, whereas immune regulatory TAMs (Reg-TAMs), marked by\n                      <jats:italic>SPP1<\/jats:italic>\n                      ,\n                      <jats:italic>MARCO<\/jats:italic>\n                      ,\n                      <jats:italic>SLC2A1<\/jats:italic>\n                      and\n                      <jats:italic>INHBA,<\/jats:italic>\n                      were enriched in p53\n                      <jats:sup>Abn<\/jats:sup>\n                      tumors. This divergent distribution highlighted a profound, p53-associated TAM heterogeneity. Clinically, high TAMs infiltration was consistently associated with worse overall survival predominantly in p53\n                      <jats:sup>Abn<\/jats:sup>\n                      or\n                      <jats:italic>TP53<\/jats:italic>\n                      <jats:sup>Mut<\/jats:sup>\n                      patients across three independent cohorts (Zhongshan Hospital, Fudan University Shanghai Cancer Center and The Cancer Genome Atlas). Furthermore, high TAMs infiltration correlated with poorer responses to both platinum-based chemotherapy and anti-programmed cell death-ligand 1 immunotherapy specifically in the p53\n                      <jats:sup>Abn<\/jats:sup>\n                      or\n                      <jats:italic>TP53<\/jats:italic>\n                      <jats:sup>Mut<\/jats:sup>\n                      subgroup. Notably, aberrant p53 status was strongly coupled with a distinct metabolic reprogramming in TAMs, favoring lipid catabolism and immunoregulatory polarization. Trajectory analysis revealed a skewed differentiation axis in p53\n                      <jats:sup>Abn<\/jats:sup>\n                      tumors toward terminally differentiated Reg-TAMs. Immunohistochemistry and flow cytometry validated increased immunosuppressive TAM subsets in p53\n                      <jats:sup>Abn<\/jats:sup>\n                      UC. Additionally, p53\n                      <jats:sup>Abn<\/jats:sup>\n                      tumors exhibited an altered CD4\n                      <jats:sup>+<\/jats:sup>\n                      T-cell landscape, enriched for suppressive subsets (regulatory, exhausted, and metallothionein-expressing T cells) coexisting with Reg-TAMs, potentially associated with immune suppression via the predicted SPP1-CD44 axis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      In UC, aberrant p53 status correlates with a remodeled TIME, characterized by metabolically reprogrammed, immunosuppressive TAMs. These TAMs co-evolve with suppressive CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells, suggesting a coordinated immunosuppressive network potentially involving SPP1-CD44 signaling. Together, this specific genotype-phenotype coupling delineates a profoundly immunosuppressive ecosystem that likely impedes immune clearance and limits therapeutic efficacy.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2025-014408","type":"journal-article","created":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T14:15:16Z","timestamp":1779286516000},"page":"e014408","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Aberrant p53 fuels macrophage immunoregulatory polarization and refractory clinical outcome in urothelial carcinoma"],"prefix":"10.1136","volume":"14","author":[{"given":"Yawei","family":"Ding","sequence":"first","affiliation":[{"name":"Department of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai, 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