{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,22]],"date-time":"2026-08-22T04:27:08Z","timestamp":1787372828373,"version":"build-2736575974"},"reference-count":36,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T00:00:00Z","timestamp":1787270400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T00:00:00Z","timestamp":1787270400000},"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"],"abstract":"Summary<\/jats:title>\n \n The 2022 European LeukemiaNet (ELN) recommendation redefined favourable\u2010risk CCAAT\/enhancer binding protein alpha (\n CEBPA<\/jats:italic>\n )\u2010mutated acute myeloid leukaemia (AML) by in\u2010frame C\u2010terminal basic leucine zipper domain (bZIP) mutations rather than double\n CEBPA<\/jats:italic>\n mutations. We analysed 411\n CEBPA<\/jats:italic>\n \u2010mutated AML patients from six Chinese centres, classified as single\u2010mutant\n CEBPA<\/jats:italic>\n bZIP\u2010other<\/jats:sup>\n (sm\n CEBPA<\/jats:italic>\n bZIP\u2010other<\/jats:sup>\n ;\n n<\/jats:italic>\n \u2009=\u200938), sm\n CEBPA<\/jats:italic>\n bZIP\u2010inf<\/jats:sup>\n (\n n<\/jats:italic>\n \u2009=\u200939), double\u2010mutant\n CEBPA<\/jats:italic>\n other<\/jats:sup>\n (dm\n CEBPA<\/jats:italic>\n other<\/jats:sup>\n ;\n n<\/jats:italic>\n \u2009=\u200937) and dm\n CEBPA<\/jats:italic>\n bZIP\u2010inf<\/jats:sup>\n (\n n<\/jats:italic>\n \u2009=\u2009297). Dm\n CEBPA<\/jats:italic>\n bZIP\u2010inf<\/jats:sup>\n patients were younger, had more de novo AML and showed distinct co\u2010mutation profiles, with more GATA binding protein 2 (\n GATA2<\/jats:italic>\n ) and fewer nucleophosmin 1 (\n NPM1<\/jats:italic>\n )\/DNA methyltransferase 3 alpha (\n DNMT3A<\/jats:italic>\n ) mutations. Additionally, dm\n CEBPA<\/jats:italic>\n bZIP\u2010inf<\/jats:sup>\n patients had a higher composite complete remission (CRc) rate (94.6% vs. 84.2%\u201389.2%,\n p<\/jats:italic>\n \u2009=\u20090.025) and better survival than the other three groups (3\u2010year overall survival [OS]: 80.0% vs. 57.4%\u201370.6%,\n p<\/jats:italic>\n \u2009<\u20090.001; 3\u2010year disease\u2010free survival [DFS]: 74.5% vs. 45.4%\u201367.9%,\n p<\/jats:italic>\n \u2009=\u20090.002). Multivariable Cox regression analysis showed that dm\n CEBPA<\/jats:italic>\n bZIP\u2010inf<\/jats:sup>\n and sm\n CEBPA<\/jats:italic>\n bZIP\u2010inf<\/jats:sup>\n had comparable survival, whereas dm\n CEBPA<\/jats:italic>\n bZIP\u2010inf<\/jats:sup>\n had better survival than sm\n CEBPA<\/jats:italic>\n bZIP\u2010other<\/jats:sup>\n and dm\n CEBPA<\/jats:italic>\n other<\/jats:sup>\n . However, among intensively treated patients, dm\n CEBPA<\/jats:italic>\n bZIP\u2010inf<\/jats:sup>\n was associated with superior survival compared with sm\n CEBPA<\/jats:italic>\n bZIP\u2010inf<\/jats:sup>\n (OS, hazard ratio [HR]\u2009=\u20091.542,\n p<\/jats:italic>\n \u2009=\u20090.017; DFS, HR\u2009=\u20091.618,\n p<\/jats:italic>\n \u2009=\u20090.014) and other two\n CEBPA<\/jats:italic>\n groups in multivariable models. Among dm\n CEBPA<\/jats:italic>\n bZIP\u2010inf<\/jats:sup>\n patients, intensive chemotherapy (HR\u2009=\u20090.51,\n p<\/jats:italic>\n \u2009=\u20090.012), adverse karyotype (HR\u2009=\u20091.52,\n p<\/jats:italic>\n \u2009=\u20090.037), age \u226550\u2009years (HR\u2009=\u20091.74,\n p<\/jats:italic>\n \u2009=\u20090.044), neuroblastoma RAS viral oncogene homolog (\n NRAS<\/jats:italic>\n ) (HR\u2009=\u20091.64,\n p<\/jats:italic>\n \u2009=\u20090.014) and colony\u2010stimulating factor 3 receptor (\n CSF3R<\/jats:italic>\n ) mutation (HR\u2009=\u20091.78,\n p<\/jats:italic>\n \u2009=\u20090.049) were independent factors for OS. No significant difference in survival was observed between patients with\n CEBPA<\/jats:italic>\n bZIP\u2010indel<\/jats:sup>\n and\n CEBP<\/jats:italic>\n bZIP\u2010ms<\/jats:sup>\n mutations. In conclusion, the dm\n CEBPA<\/jats:italic>\n bZIP\u2010inf<\/jats:sup>\n subgroup displayed unique co\u2010mutation gene spectra and had better prognoses among the intensive treated cohort.\n <\/jats:p>","DOI":"10.1111\/bjh.70786","type":"journal-article","created":{"date-parts":[[2026,8,22]],"date-time":"2026-08-22T04:03:36Z","timestamp":1787371416000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Enhanced prognosis of acute myeloid leukaemia patients with\n \n dm\n CEBPA<\/i>\n bZIP<\/sup>\n <\/scp>\n \u2010inf<\/sup>\n mutations: Insights from a multicentre Chinese cohort study"],"prefix":"10.1111","author":[{"given":"Guanghui","family":"Chang","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 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5626-3366","authenticated-orcid":false,"given":"Pengcheng","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Hematology Nanfang Hospital, Southern Medical University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7352-9560","authenticated-orcid":false,"given":"Liping","family":"Dou","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Experimental Hematology The Fifth Medical Center of PLA General Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinhai","family":"Ren","sequence":"additional","affiliation":[{"name":"Department of Hematology The Second Hospital of Hebei Medical University, Hebei Key Laboratory of Hematology Shijiazhuang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongyu","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Hematology Peking University Shenzhen Hospital Shenzhen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7131-0522","authenticated-orcid":false,"given":"Qian","family":"Jiang","sequence":"additional","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 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hao","family":"Jiang","sequence":"additional","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 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0267-1081","authenticated-orcid":false,"given":"Lanping","family":"Xu","sequence":"additional","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 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaohui","family":"Zhang","sequence":"additional","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 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2145-6643","authenticated-orcid":false,"given":"Xiaojun","family":"Huang","sequence":"additional","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 China"},{"name":"Peking\u2010Tsinghua Center for Life Sciences, Academy for Advanced Interdisciplinary Studies Peking University Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6294-972X","authenticated-orcid":false,"given":"Suning","family":"Chen","sequence":"additional","affiliation":[{"name":"National Clinical Research Center for Hematologic Diseases The First Affiliated Hospital of Soochow University, Institute of Blood and Marrow Transplantation Soochow China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0460-9887","authenticated-orcid":false,"given":"Feifei","family":"Tang","sequence":"additional","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 China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,8,21]]},"reference":[{"issue":"4","key":"e_1_2_10_2_1","doi-asserted-by":"crossref","first-page":"1267","DOI":"10.1182\/blood-2003-02-0477","article-title":"Transcription activation function of C\/EBPalpha is required for induction of granulocytic differentiation","volume":"102","author":"Keeshan 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