{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T11:56:45Z","timestamp":1791806205111,"version":"4.3.4"},"reference-count":32,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2025,11,30]],"date-time":"2025-11-30T00:00:00Z","timestamp":1764460800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,11,30]],"date-time":"2025-11-30T00:00:00Z","timestamp":1764460800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Br J Haematol"],"published-print":{"date-parts":[[2026,2]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    This study aimed to investigate the distinct clinical characteristics and molecular features of\n                    <jats:italic>TP53<\/jats:italic>\n                    \u2010mutant acute myeloid leukaemia (AML) patients. We retrospectively analysed 193\n                    <jats:italic>TP53<\/jats:italic>\n                    \u2010mutant AML patients. Better responses were observed in patients treated with the venetoclax in combination with hypomethylating agent (VEN\u2009+\u2009HMA) regimen compared to those receiving the \u2018\n                    <jats:italic>3\u2009+\u20097<\/jats:italic>\n                    \u2019 regimens (composite complete remission [CRc], 53.8% vs. 30.2%;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.018).\n                    <jats:italic>TP53<\/jats:italic>\n                    V272 mutation was associated with a lower relapse rate (0% vs. 35.2%;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.041). The single hit group exhibited superior OS compared to the multi\u2010hit group (the median overall survival [OS]: 14.3\u2009months vs. 10.8\u2009months;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.029).\n                    <jats:italic>TP53<\/jats:italic>\n                    \u2010mutant AML patients with\n                    <jats:italic>CEBPA bZIP in\u2010frame<\/jats:italic>\n                    mutations showed prolonged OS (the median OS: 25.2\u2009months vs. 13.8\u2009months;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.036). Better prognoses were also shown in patients with\n                    <jats:italic>RUNX1\u2010RUNX1T1<\/jats:italic>\n                    fusion gene (the median OS: 31.1\u2009months vs. 13.7\u2009months;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.002). Multivariate analysis identified three significant prognostic factors for OS:\n                    <jats:italic>RUNX1\u2010RUNX1T1<\/jats:italic>\n                    fusion gene (hazard ratio [HR]\u2009=\u20090.23, 95% confidence interval [CI], 0.08\u20130.63;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.005),\n                    <jats:italic>RUNX1<\/jats:italic>\n                    mutation (HR\u2009=\u20091.84; 95% CI, 1.14\u20132.96;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.012) and\n                    <jats:italic>FLT3\u2010ITD<\/jats:italic>\n                    mutation (HR\u2009=\u20093.14; 95% CI, 1.80\u20135.47;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.001). In conclusion, molecular factors matter in influencing the prognosis of\n                    <jats:italic>TP53<\/jats:italic>\n                    \u2010mutant AML patients. Among them,\n                    <jats:italic>TP53<\/jats:italic>\n                    mutation sites merit particular attention.\n                  <\/jats:p>","DOI":"10.1111\/bjh.70271","type":"journal-article","created":{"date-parts":[[2025,12,1]],"date-time":"2025-12-01T06:44:02Z","timestamp":1764571442000},"page":"579-588","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Decoding the molecular drivers of\n                    <i>TP53<\/i>\n                    \u2010mutant acute myeloid leukaemia: Clinical implications and prognostic insights"],"prefix":"10.1111","volume":"208","author":[{"given":"Lin\u2010Ya","family":"Wang","sequence":"first","affiliation":[{"name":"Peking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies Peking University  Beijing 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