Experimental Hematology & Oncology最新文献

{"title":"Long-term extended-interval teclistamab and talquetamab dosing without step-up dosing in previously treated multiple myeloma.","authors":"Callee Brooks, Leslie Mader, Kathryn Kennedy, Phyu Thin Naing, Salyka Sengsayadeth, Bhagirathbhai Dholaria, Adetola Kassim, Sarah Profitt, Muhamed Baljevic","doi":"10.1186/s40164-026-00816-x","DOIUrl":"10.1186/s40164-026-00816-x","url":null,"abstract":"<p><p>Teclistamab (Tec) and talquetamab (Tal) are bispecific CD3 T-cell engagers targeting B-cell maturation antigen and G protein-coupled receptor, class C, group 5, member D, respectively, and have transformed how we treat relapsed/refractory multiple myeloma (RRMM). Early onset toxicities, such as cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS), require utilization of pre-medications, step-up dosing (SUD) schemas, and close monitoring while late onset toxicities, such as hypogammaglobulinemia, myelosuppression, and notably infections, can lead to significant complications and treatment interruptions, which may require extending bispecific antibody (BsAb) dosing intervals to mitigate toxicities. While current prescribing information for Tec and Tal recommend repeat SUD for prolonged dose delays, we report a series of six patients (pts) who continued therapy with extended dosing intervals (EDI) (8-12 weeks) without repeating SUD. Notably, all pts had achieved a  ≥  complete response (CR) prior to transitioning to extended interval dosing, which was chosen either to improve tolerability or per provider preference based on depth of disease response. Despite experiencing CRS (83% of pts) and ICANS (17% of pts) during their initial SUD, no CRS or ICANS events occurred after 23 doses of Tec/Tal given at EDI, despite a median duration between doses of 77 days. At the time of this report, all patients in this cohort have sustained, deep disease response and remain on BsAb therapy. Despite small sample size, this report adds to limited available data supporting safe and feasible omission of SUD in RRMM pts slated for Tec/Tal therapy resumption via EDI.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"15 1","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13471332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148722158","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":"Sequential therapy with decitabine and an XPO-1 inhibitor followed by allogeneic hematopoietic stem cell transplantation in MDS with biallelic TP53 inactivation patients : a preliminary case series.","authors":"Yanling Ren, Wei Lang, Yu Xu, Chen Mei, Xianbo Huang, Shasha Wang, Jiejing Qian, Hongyan Tong","doi":"10.1186/s40164-026-00817-w","DOIUrl":"10.1186/s40164-026-00817-w","url":null,"abstract":"<p><p>Myelodysplastic syndrome with biallelic TP53 inactivation (MDS-biTP53) patients represents an ultra-high-risk subgroup with dismal outcomes. Even after allogeneic hematopoietic stem cell transplantation (allo-HSCT), relapse rates remain extremely high and survival is poor. This preliminary case series reports the outcomes of 8 consecutive patients with MDS-biTP53 who received a novel sequential therapy of decitabine (DAC) combined with the XPO-1 inhibitor selinexor, followed by allo-HSCT at a single center between September 2024 and December 2025. At a median follow-up of 7.3 months (95% CI, 4.2-10.4 months) from HSCT, median overall survival (OS) and relapse-free survival (RFS) were not reached. At last follow-up, 7/8 patients remained alive (OS 87.5%) and 6/8 were relapse-free (RFS 75%), with one relapse (12.5%). This patient successfully achieved a second complete remission following preemptive therapy with low-dose decitabine combined with donor lymphocyte infusion and remained in remission at the last follow-up. Two patients developed serious infections during the peritransplant period. One patient with pre-transplant intestinal colonization of carbapenem-resistant Enterobacteriaceae (CRE) ultimately died due to CRE bloodstream infection followed by intestinal graft-versus-host-disease (GVHD). Overall treatment-related toxicity was deemed manageable, and the incidence of grade III-IV acute GVHD was 25% (2/8). This preliminary study provides encouraging evidence that sequential decitabine and selinexor therapy followed by allo-HSCT may improve outcomes with acceptable toxicity in patients with ultra-high-risk MDS-biTP53. However, these findings are limited by the small sample size, relatively short follow-up, and retrospective, single-center design. Confirmation in larger prospective trials is warranted.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"15 1","pages":""},"PeriodicalIF":17.5,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13455397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705952","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":"AAV-delivered miRNA-gated Cre circuits enable programmable gene activation in AFP-active liver tumor models.","authors":"Xiaoting Zhang, Congcong Cao, Zeqi Huang, Dongde Wu, Tao Yin, Yuchen Liu, Jian Shen, Aolin Li, Shuofei Yang, Lei Nie","doi":"10.1186/s40164-026-00814-z","DOIUrl":"10.1186/s40164-026-00814-z","url":null,"abstract":"<p><p>Selective therapeutic gene activation in tumors remains challenging because tumor-enriched promoters often exhibit basal activity in non-target cells and may not fully capture intratumoral heterogeneity. In addition, direct promoter-driven expression of cytotoxic or tumor-suppressive payloads may be vulnerable to promoter leakiness, which can compromise specificity and safety. Here, we developed SLICER, a two-vector adeno-associated virus (AAV)-delivered Cre-loxP gene circuit that integrates an alpha-fetoprotein (AFP) promoter-driven sensor with post-transcriptional gating through microRNA (miRNA) recognition elements (MREs) for miR-21 and miR-122. This dual-layer design separates tumor-context sensing from downstream payload activation, converting context-dependent Cre accumulation into recombination-gated payload expression from the actuator vector. In AFP-active liver tumor cell models, including HepG2, Huh7, and PLC/PRF/5, SLICER induced robust Cre expression and loxP-dependent luciferase activation, whereas non-target/comparator cells showed minimal background activity and limited functional toxicity. Mutation of miR-21 and/or miR-122 recognition elements increased Cre accumulation and reporter output, supporting an MRE-dependent gating mechanism that contributes to circuit specificity. A pro-apoptotic BAX payload triggered caspase-dependent apoptosis in target cells, which was partially attenuated by Z-VAD-FMK, while non-target cells remained largely unaffected. Perturbation of miRNA inputs further tuned circuit output, consistent with miRNA-guided regulation. SLICER also accommodated modular tumor-suppressor payloads, including TP53 and PTEN, supporting actuator-layer interchangeability. In vivo, systemic AAV delivery of SLICER-TP53 suppressed tumor growth and reduced tumor burden in both HepG2 and Huh7 xenograft models, accompanied by increased intratumoral P53 expression. Together, these findings establish SLICER as a modular proof-of-concept platform for combinatorial transcriptional and post-transcriptional control of therapeutic gene activation in AFP-active liver tumor contexts, while supporting further development of logic-gated gene circuits for more precise tumor-selective payload delivery.</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/PMC13452114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148697265","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":"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}