Experimental Hematology & Oncology最新文献

{"title":"Cellular adhesion-dependent 3D morphogenesis indicating brain tumor aggressiveness and chemosensitivity in spherical cavity culture.","authors":"Thuy Huynh, Jieun Kim, Sarnai Amartumur, Inhee Choi, Ji Yeoun Lee, Luke P Lee, Chaejeong Heo","doi":"10.1186/s40164-026-00785-1","DOIUrl":"10.1186/s40164-026-00785-1","url":null,"abstract":"<p><p>Malignancies of the nervous system remain a critical challenge in oncology, contributing substantially to cancer-related mortality in children and adults. Their aggressive behavior is influenced by adhesion heterogeneity of the tumor cells, as distinct patterns of cell-to-cell and cell-to-matrix interactions shape tumor organization, invasion, and resistance to conventional treatments. Here, we investigate tumor adhesion dynamics in a 3D spherical cavity culture platform that enables the rapid and high-throughput formation of uniform spheroids for parallel morphogenesis, adhesion profiling, and drug screening. The morphogenetic patterns of human neuroblastoma and patient-derived glioblastoma observed in 3D cavity culture closely correlated with tumor aggressiveness, ranging from adhesive layers in benign tumor subtype to compact spheroids in malignant cells and irregular aggregates in highly invasive, cancer stem-like counterparts. These morphologies corresponded to adhesion profiles: aggressive cells displayed elevated N-cadherin with variable integrin, while compact spheroids maintained a balance of both molecules. Blocking N-cadherin with ADH-1 disrupted spheroid integrity, and combining ADH-1 with DOX yielded synergistic cytotoxic effects in malignant phenotypes, highlighting N-cadherin upregulation in tumor cells with higher aggressiveness in 3D culture. Overall, our dynamic 3D spherical cavity culture enables reproducible 3D adhesion phenotyping, providing a simple method for malignancy assessment and supporting adhesion-targeted therapeutic strategies for personalized medicine.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"15 1","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13452115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148697305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The spatial and multi-omic landscape of Down syndrome leukemogenesis: moving beyond cellular heterogeneity.","authors":"Edoardo Peroni, Rosario Amato, Martina Bado, Mosè Favarato, Antonio Rosato","doi":"10.1186/s40164-026-00815-y","DOIUrl":"10.1186/s40164-026-00815-y","url":null,"abstract":"<p><p>Down syndrome (DS) confers a developmentally rooted predisposition to both myeloid and lymphoid leukemias, particularly myeloid leukemia associated with DS (ML-DS) and acute lymphoblastic leukemia associated with DS (ALL-DS). While trisomy 21-driven gene dosage imbalance is central to this risk, DS leukemogenesis cannot be fully explained by recurrent mutations alone; it reflects a dynamic interplay between altered hematopoietic development, cell-intrinsic programs, and tissue microenvironmental cues. In this perspective, we argue that the field should move beyond cataloging cellular heterogeneity and adopt a topographic, multi-omic framework of DS leukemogenesis. We discuss how fetal niche biology shapes pre-leukemic evolution in ML-DS, including the developmental context of GATA1-mutant clones, and how therapy-driven bottlenecks may promote persistence of spatially protected residual disease in ALL-DS. We further highlight the translational potential of integrating spatially resolved transcriptomics with single-cell and protein-aware multi-omics to identify compartment-specific signaling programs and clinically actionable vulnerabilities. A spatially informed model of DS leukemia may improve biological stratification, clarify mechanisms of relapse and toxicity, and support the development of more effective and less toxic therapeutic strategies.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"15 1","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatially resolved transcriptomic profiling of myelofibrosis spleen reveals compartment specific niche programs.","authors":"Edoardo Peroni, Marco Pizzi, Marco Basso, Alessandro Atanasio, Elisabetta Calistri, Michele Gottardi, Antonio Rosato","doi":"10.1186/s40164-026-00811-2","DOIUrl":"10.1186/s40164-026-00811-2","url":null,"abstract":"<p><p>Myelofibrosis (MF) splenomegaly reflects not only extramedullary hematopoiesis (EMH) but a compartmental organization of the splenic microenvironment into spatially distinct niches. Using Spatial whole transcriptome profiling on FFPE spleen tissue from three MF patients, we interrogated three anatomically defined compartments: Intravascular (IV), Perivascular (PV) and Red Pulp (RP). Differential expression was estimated through pairwise compartment contrasts with Benjamini-Hochberg false discovery rate correction (FDR < 0.05, |log2FC|≥1), and compartment \"core signatures\" were defined by directional concordance across the two contrasts relevant to each compartment. IV regions of interest (ROIs) showed an endothelial/adhesion and vascular stress program (e.g., PECAM1, VCAM1; antioxidant enzymes). PV ROIs were characterized by fibro-remodeling and immune-structured signals (COL1A1/COL3A1, LOXL1, MMP2/TIMP1; HLA‑DRA/CD74) including CXCL12, consistent with a PV niche coupling extracellular matrix remodeling to hematopoietic retention cues. RP ROIs captured an EMH-associated erythroid/heme program (ALAS2, FECH, BLVRB) with stress and inflammatory alarmins (S100A8/S100A9). Together, these findings support a compartmental \"division of labor\" in MF spleen, vascular interface activation, PV remodeling/chemokine niches, and RP EMH/redox stress, providing a spatial framework to interpret splenomegaly as structured niche dependencies and to prioritize candidate microenvironmental dependencies for follow‑up validation.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"15 1","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13430905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148668815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging agents and regimens for myeloproliferative neoplasms: updates from ASH 2025 Annual Meeting.","authors":"Tiantian Zhang, Heng Jiang, Delong Liu","doi":"10.1186/s40164-026-00813-0","DOIUrl":"10.1186/s40164-026-00813-0","url":null,"abstract":"<p><p>Current Myeloproliferative neoplasm (MPN) therapies provide meaningful symptom and event-risk control but are limited by infrequent molecular remissions, treatment-limiting cytopenias (particularly anemia), and continued reliance on non-mutation-directed cytoreduction or phlebotomy with attendant morbidity. At ASH 2025 Annual Meeting, multiple investigational strategies aimed to address these limitations, including clone-directed targeting (INCA033989), phlebotomy-sparing physiologic therapy (rusfertide), and epigenetic disease-modifying combinations (pelabresib). We summarized the latest updates on these emerging agents and regimens for MPNs from the 2025 ASH Annual Meeting.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"15 1","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13430699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148668789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Arsenic trioxide promotes a glue‑like interaction to drive STUB1-mediated NPM-ALK degradation in ALK⁺ ALCL.","authors":"Guiming Li, Jun Wang, Shiguang Ye, Lixin Zhou, Yanli Sun, Bowen Li, Yunshuo Zhao, Yi Ding, Yu Zeng, Bin Xue, Guangming Wang, Fangce Wang, Xiu Luo, Aibin Liang, Ellen L Weisberg, Wenjun Zhang, Wenchao Lu, Jing Yang","doi":"10.1186/s40164-026-00800-5","DOIUrl":"10.1186/s40164-026-00800-5","url":null,"abstract":"<p><p>The nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) fusion constitutively activates ALK tyrosine kinase, driving oncogenesis in anaplastic large cell lymphoma (ALCL). While arsenic trioxide (ATO) exhibits therapeutic potential, its precise mechanism remains elusive, limiting clinical application. Here, we used a combined approach of E3 ligase library screening, ATO chemical proteomics, and NPM-ALK immunoprecipitation-mass spectrometry to reveal that ATO regulates NPM-ALK stability via the E3 ligase STUB1. Clinically, high STUB1 expression correlates with improved survival, identifying it as a candidate favorable prognostic biomarker in NPM-ALK⁺ ALCL. Mechanistically, ATO promotes a glue‑like interaction that stabilizes the ternary complex of STUB1 and NPM-ALK, promoting ubiquitination at K174 and subsequent proteasomal degradation. Furthermore, structural modeling, domain mapping, and point mutations support a proposed arsenic-dependent interaction model involving STUB1 Cys83, Cys103, and NPM-ALK Cys599, which may modulate the STUB1-NPM-ALK interface and enhance their interaction, thereby promoting ubiquitin-mediated degradation. Crucially, we demonstrate that STUB1 overexpression or pharmacological activation using the FDA-approved cardiac glycoside Deslanoside synergizes profoundly with ATO to inhibit tumor growth both in vitro and in vivo. These findings provide novel mechanistic insight into ATO's action in NPM-ALK⁺ ALCL and reveal new therapeutic strategies and candidate prognostic biomarkers for patient management.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"15 1","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13421824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148629876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging venetoclax plus hypomethylating agent-based triplet regimens in newly diagnosed acute myeloid leukemia: updates from the 2025 ASH Annual Meeting.","authors":"Haibo Yu, Ting Shi, Hong-Hu Zhu","doi":"10.1186/s40164-026-00810-3","DOIUrl":"10.1186/s40164-026-00810-3","url":null,"abstract":"<p><p>Venetoclax (VEN) combined with a hypomethylating agent (HMA) has become a standard-of-care frontline therapy for unfit patients with newly diagnosed acute myeloid leukemia (ND AML). The VIALE-A trial established the clinical benefit of VEN plus azacitidine (AZA), with a composite complete remission rate (CRc) of 66.4% and a median overall survival (OS) of 14.7 months. Nevertheless, remission durability remains heterogeneous, and the regimen is non-curative for many patients. Improving remission rates and long-term survival therefore remains an urgent unmet clinical need. VEN/HMA-based triplet regimens incorporating targeted agents are emerging as promising strategies in ND AML, particularly FLT3 inhibitor-based combinations reported at the 2025 American Society of Hematology (ASH) Annual Meeting. Notably, longer-term follow-up data from a study of gilteritinib plus VEN/AZA in patients with ND FLT3-mutated AML showed a median OS of 29.7 months. Additional VEN/HMA-based strategies, including combinations with menin inhibitors and other novel agents, are also being investigated. Here, we provide an overview of the latest clinical updates on VEN/HMA-based triplet regimens in ND AML presented at the 2025 ASH Annual Meeting.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"15 1","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13404094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Frontline T cell-redirecting therapies in newly diagnosed multiple myeloma: key signals from the 2025 ASH Annual Meeting.","authors":"Huixing Zhou, Xiaoyun Jin, Wenming Chen, Hong-Hu Zhu, Wen Gao","doi":"10.1186/s40164-026-00809-w","DOIUrl":"10.1186/s40164-026-00809-w","url":null,"abstract":"<p><p>Early frontline data presented at the 2025 ASH Annual Meeting suggest that T cell-redirecting strategies, including chimeric antigen receptor (CAR)-T cells and bispecific antibodies (BsAbs), can induce rapid, high rates of minimal residual disease (MRD)-negative responses in newly diagnosed multiple myeloma (NDMM), including transplant-ineligible (TI) and high-risk populations. However, short follow-up, heterogeneous MRD methodologies, and infection risk-particularly with continuous bispecific exposure-underscore that these approaches remain investigational and should be advanced through randomized, MRD-guided fixed-duration trials.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"15 1","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13383529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimizing the timing of JAK1 inhibition preserves the anti-tumor efficacy of radioimmunotherapy in lung cancer by preventing T cell exhaustion.","authors":"Zhiru Gao, Linlin Yang, Linlin Wang","doi":"10.1186/s40164-026-00802-3","DOIUrl":"10.1186/s40164-026-00802-3","url":null,"abstract":"<p><p>JAK1 inhibitors are widely used in hematologic malignancies and autoimmune diseases, their potential in combination with immunotherapy for solid tumors such as lung cancer is increasingly being recognized. The combination of radiotherapy and immunotherapy (radioimmunotherapy, iRT) has become a standard treatment strategy for lung cancer, but the impact of JAK1 inhibitors on the antitumor efficacy of iRT remains insufficiently explored. This study aimed to investigate the anti-tumor effects of JAK1 inhibition on iRT and the underlying mechanisms. The direct effects of JAK1 inhibitor on lung cancer were evaluated in vitro using cell proliferation, colony formation, and wound healing assays, and in vivo using immunodeficient mouse models. In addition, in immunocompetent mouse models of subcutaneous and orthotopic lung tumors, we analyzed the influence of JAK1 inhibitor on the tumor immune microenvironment during iRT, with a focus on the T-cell function. The results revealed that although JAK1 inhibitor monotherapy markedly suppressed lung tumor growth, its concurrent administration unexpectedly compromised the antitumor efficacy of iRT, an effect associated with impaired CD8⁺ T cell activity and interferon-γ (IFN-γ) production. In contrast, short-term delayed administration of the JAK1 inhibitor approximately one week after completing iRT was found to mitigate T-cell exhaustion, optimize immune responses, and thereby preserve the antitumor efficacy of iRT. In conclusion, concurrent use of JAK1 inhibitor during iRT should be avoided in lung cancer treatment. Optimizing the timing of JAK1 inhibition represents a promising strategy to mitigate immunosuppression while maintaining therapeutic efficacy.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"15 1","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13383407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cystathionine beta-synthase promotes anoikis resistance and transcoelomic metastasis in ovarian cancer via SP1- ITGB1 regulation.","authors":"Pallab Shaw, Arpan Dey Bhowmik, Akrit Pran Jaswal, Rameswari Velayutham, Srikanth Chiliveru, Samantha Ricketts, Chao Xu, Danny N Dhanasekaran, Zhizhaung Joe Zhao, Resham Bhattacharya, Priyabrata Mukherjee, Shailendra Kumar Dhar Dwivedi, Geeta Rao","doi":"10.1186/s40164-026-00808-x","DOIUrl":"10.1186/s40164-026-00808-x","url":null,"abstract":"<p><p>Anoikis resistance is crucial for ovarian cancer (OvCa) transcoelomic metastasis, during which exfoliated OvCa cells survive as spheroids before invading the omentum. Here, we demonstrate that cystathionine β-synthase (CBS), an H₂S-producing transsulfuration pathway enzyme, is a key determinant of OvCa spheroidal viability and metastatic potential. Analysis of publicly available patient datasets, as well as an in-house tissue microarray, revealed that high CBS expression positively correlates with both poor progression-free survival and clinically observed peritoneal/omental metastasis. Integrated functional and proteomic analyses indicated that CBS silencing induces apoptosis in 2D monolayers. Consistent with this, CBS silencing in spheroids caused apoptosis and disrupted spheroid architecture. Mechanistically, this phenotype was associated with downregulation of oncogenic stemness and epithelial-mesenchymal transition. Further, through proteomic and bioinformatic analyses, we identified ITGB1 to be the hub protein in OvCa spheroidogenesis. Interestingly, knockdown of CBS led to abrogation of the ITGB1-mediated downstream pathway. Moreover, by proteomic and network analyses, we identified SP1 as a key transcriptional regulator of CBS-induced pro-spheroidal transcriptional programs of stemness and invasiveness. Stabilization of SP1 through persulfidation by H₂S supplementation restored spheroidal viability and underlying protein signaling. Further, our results reveal that loss of CBS, through ITGB1 repression, disrupts spheroid architecture, leading to reduced metastatic docking on the murine omental surface in vivo. Collectively, these findings identify CBS as a central regulator of anoikis resistance and OvCa transcoelomic metastasis, highlighting the therapeutic potential of targeting CBS-dependent SP1-ITGB1 regulation to control metastatic spread.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":" ","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13579884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148420137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autologous transplant versus matched sibling donor transplant in intermediate-risk AML in CR1 with no detectable MRD: a biological assignment comparative study.","authors":"Sijian Yu, Hui Liu, Weihua Zhao, Guopan Yu, Pengcheng Shi, Danian Nie, Zhiqiang Sun, Qianwei Liu, Ruoyang Shao, Zinan Feng, Xinquan Liang, Xiong Zhang, Xin Du, Xiaojun Xu, Shunqing Wang, Qing Zhang, Yirong Jiang, Hongyu Zhang, Ziwen Guo, Min Dai, Xuejie Jiang, Dan Xu, Fen Huang, Zhiping Fan, Na Xu, Qiong Liu, Qianyi Liang, Can Liu, Meiqing Wu, Guangyang Weng, Ren Lin, Hua Jin, Jing Sun, Yu Wang, Li Xuan, Yu Zhang, Qifa Liu","doi":"10.1186/s40164-026-00807-y","DOIUrl":"10.1186/s40164-026-00807-y","url":null,"abstract":"<p><strong>Background: </strong>Retrospective studies suggested that autologous stem cell transplantation (auto-SCT) might achieve comparable or even better outcomes compared with allogeneic SCT for patients with genetic intermediate-risk acute myeloid leukemia (IR-AML) and no detectable measurable residual disease (MRD-). However, prospective studies are lacking comparing auto-SCT and matched sibling donor SCT (MSD-SCT).</p><p><strong>Patient and methods: </strong>We initiated a biological assignment comparative study at fourteen institutions in China. Patients with newly diagnosed de novo IR-AML and MRD- within 3 cycles of intensive chemotherapy were eligible for the study if they were 14 to 60 years old and received auto-SCT or MSD-SCT. Patients were assigned to auto-SCT or MSD-SCT based on donor availability. The primary endpoint was the 3-year disease-free survival (DFS). The trial was registered with Clinicaltrials.gov, NCT03620955 and completed.</p><p><strong>Results: </strong>Between November 15, 2018, and March 31, 2022, 708 patients were screened and 518 eligible for analysis, including 259 in the auto-SCT and 259 in the MSD-SCT groups. With a median follow-up time of 55.2 (IQR 47.4-65.2) months, the 3-year DFS was 82.2% (95% CI 77.0-86.4) and 85.7% (95% CI 80.8-89.4) in auto-SCT and MSD-SCT respectively (HR, 1.24 [95% CI, 0.81-1.91]; p=.32). The treatment-adjusted difference was 3.2% (95% CI, - 3.1 to 9.4; p<.001). Because the upper bound of the 95% CI (9.4) did not exceed 10%, noninferiority was shown. The 3-year overall survival (OS) was 90.7% (95% CI 86.5-93.7) and 87.6% (95% CI 83.0-91.1) respectively (HR, 0.78 [95% CI, 0.47-1.30]; p=.34). In subgroup analyses, auto-SCT achieved similar DFS and OS to MSD-SCT among patients who reached MRD- in the first 2 cycles of chemotherapy, while auto-SCT had inferior DFS but similar OS for patients who achieved MRD- after 3 cycles.</p><p><strong>Conclusions: </strong>Auto-SCT achieved non-inferior DFS and similar OS compared with MSD-SCT, suggesting that auto-SCT is a viable and preferable first-line choice for IR-AML patients achieving MRD- within 3 cycles of chemotherapy, particularly those who reached MRD- in the first 2 cycles.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":" ","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13428435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148396468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}