Journal of Hematology & Oncology血液学与肿瘤学杂志
Journal of Hematology & Oncology(英文缩写 J HEMATOL ONCOL),ISSN 1756-8722,eISSN 1756-8722,中文译名:血液学与肿瘤学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
Journal of Hematology & Oncology 最新收录文献
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1. Mitochondrial genetic variation as a novel predictor of graft-versus-host disease after stem-cell transplantation in myelodysplastic neoplasms.
1. 线粒体遗传变异作为骨髓增生异常肿瘤中干细胞移植后移植物抗宿主病的新型预测因素PMID:日期:2026-10-01Graft-versus-host disease (GvHD) remains a major cause of morbidity and non-relapse mortality after allogeneic hematopoietic cell transplantation. Building on prior evidence implicating mitochondrial DNA (mtDNA) variation in myelodysplastic neoplasms (MDS), we investigated the prognostic impact of recipient and donor mtDNA variation on acute and chronic GvHD. Whole‑genome sequencing was performed on pretransplant samples from 494 MDS donor-recipient pairs (discovery cohort) from the Center for International Blood and Marrow Transplant Research (CIBMTR). Associations between mtDNA variations and acute GvHD grades II-IV (aGvHD24), grades III-IV (aGvHD34), and chronic GvHD (cGvHD) were assessed using cause-specific Cox proportional hazards models. Model discrimination was quantified using area under the curve (AUC). Findings were evaluated in an independent cohort of 295 MDS using targeted mtDNA deep sequencing. Among the recipient mtDNA gene associations identified in the discovery cohort, MT-ND2 for aGvHD34 (p = 1.1 × 10) and MT-CYB for cGvHD (p = 3.6 × 10) were independently validated, while MT-CO2, which was nominally associated with aGvHD34 in the discovery cohort, was also significant in the recipient validation cohort (p = 3.2 × 10). Incorporating recipient mtDNA genes into the CIBMTR aGvHD Risk Index improved discrimination for aGvHD34 by 11% (p = 0.009). In conclusion, mtDNA variants may provide independent prognostic information for GvHD and may enhance current risk stratification when integrated with standard clinical parameters.
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2. Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.
2. 癌症中的细胞衰老与调控性细胞死亡：机制、交叉调控网络及治疗意义PMID:日期:2026-09-29Cellular senescence and regulated cell death represent two fundamental but intricately connected biological programs that govern tumor cell fate. Cellular senescence can suppress tumor growth by inducing stable cell-cycle arrest and promoting immune clearance, but persistent senescent cells may also drive tumor progression through the senescence-associated secretory phenotype (SASP). Concurrently, multiple modalities of regulated cell death-including apoptosis, ferroptosis, cuproptosis, necroptosis, pyroptosis, parthanatos, and autophagy-dependent cell death-have emerged as critical determinants of therapeutic response. The crosstalk between senescence and cell death is orchestrated by key molecular hubs including p53, mitochondria, autophagy machinery, and epigenetic regulators. In this review, we summarize the hallmarks and classification of cellular senescence in cancer, outline major cell death modalities, discuss the cross-regulatory networks linking senescence and death, and highlight emerging therapeutic strategies that target these interconnected processes for cancer treatment.
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3. Targeting cancer-associated fibroblasts: therapeutic strategies, translational challenges, and future perspectives.
3. 靶向癌症相关成纤维细胞：治疗策略、转化挑战与未来展望PMID:日期:2026-09-29Cancer-associated fibroblasts (CAFs) act as key drivers of cancer progression and therapeutic resistance within the tumor microenvironment, but their diverse and context-dependent functions complicate therapeutic targeting. The limited clinical efficacy of CAF-targeting therapeutics has prompted a critical reassessment of CAF biology, therapeutic development, and emerging CAF-directed strategies. Unlike prior reviews that predominantly focused on CAF heterogeneity or isolated therapeutic modalities, this review systematically compares pharmacological and biologic CAF-targeting therapeutics, multifunctional nanomedicines, and biologically inspired and living platforms in terms of their underlying mechanisms of action and translational bottlenecks. Drawing on clinical evidence from CAF-targeting therapeutics, we identify several interconnected barriers to successful translation, including CAF heterogeneity and plasticity, patient-selection and biomarker limitations, preclinical-clinical mismatch and combination-treatment dependency, insufficient tumor penetration and systemic toxicity, and signaling redundancy and pathway compensation. Importantly, lessons from unsuccessful clinical trials are used to critically reassess whether current CAF-targeting nanomedicines and platforms adequately address these barriers. In parallel, we evaluate platform-specific translational challenges, particularly those related to biosafety and manufacturing feasibility. These analyses highlight the persistent gaps between the evolving understanding of CAF functional states, existing design rationales for nanomedicine and platforms, and real-world clinical practice. Future directions should therefore prioritize the identification of functionally defined CAF states, the optimization of clinically relevant models of advanced disease, and the development of therapeutic platforms tailored to clearly defined clinical needs. Finally, we propose an iterative translational roadmap and a hypothesis-generating sequential cancer cell/CAF dual-targeting framework to guide the development of clinically translatable CAF-directed therapies.
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4. Next-generation antibody-based therapeutics in cancer: antibody-drug conjugates bispecific antibodies across hematologic malignancies and solid tumors.
4. 癌症中的下一代抗体疗法：跨越血液系统恶性肿瘤和实体瘤的抗体偶联药物和双特异性抗体PMID:日期:2026-09-09The therapeutic paradigm in oncology is undergoing a profound transformation driven by antibody-drug conjugates (ADCs) and bispecific antibodies (bsAbs). This review comprehensively summarizes recent clinical advances of these platforms across both hematologic malignancies and solid tumors. ADCs such as trastuzumab deruxtecan have expanded the concept of targetable HER2 expression, demonstrating meaningful intracranial activity and redefining standards of care in HER2-low breast cancer and beyond. The landscape continues to broaden with novel ADC targets (TROP2, CLDN18.2, B7-H3, HER3) and bispecific ADC constructs. Concurrently, T‑cell-engaging bsAbs-CD20×CD3 in B‑cell lymphomas, BCMA×CD3 and GPRC5D×CD3 in multiple myeloma, and CD19×CD3 in acute lymphoblastic leukemia-have achieved deep and durable responses in heavily pretreated populations. In solid tumors, EGFR‑MET and DLL3‑targeted bsAbs have delivered clinically validated efficacy in historically refractory settings, including regulatory approval of tarlatamab. Despite these successes, critical challenges persist, including the management of unique toxicity profiles, the emergence of resistance via antigen escape and T‑cell exhaustion, and the absence of validated predictive biomarkers. Optimal sequencing of these agents with one another and with chimeric antigen receptor T‑cell therapy remains largely empirical. Next‑generation strategies-bispecific ADCs, probody‑drug conjugates, and immune‑stimulating antibody conjugates-combined with immunotherapy partnerships hold promise for overcoming resistance and improving therapeutic indices. By distilling pivotal clinical data and highlighting unresolved questions, this review provides a roadmap for translating antibody‑based innovations into precision oncology.
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5. Cytokine fusion proteins for solid tumor therapy: mechanistic insights and clinical advances.
PMID:日期:2026-09-05Cytokine fusion proteins are engineered biologics that combine functional modules, such as cytokines, antibodies, or albumin-binding domains, into a single molecular entity. These agents have emerged as promising therapeutic platforms for treating solid tumors. However, their clinical translation remains constrained by the need to achieve potent antitumor activity while mitigating dose-limiting systemic toxicities. Here, we dissect the mechanistic foundations of cytokine fusion protein function by examining key cytokine signaling pathways within the tumor microenvironment. We also provide a comprehensive overview of current engineering strategies and clinical developments, focusing on approaches to optimize pharmacokinetics, enhance tumor-targeted delivery, and achieve therapeutic synergy. Collectively, this Review summarizes the evolving landscape of cytokine fusion protein development and discusses emerging opportunities and challenges that may inform future advances in this field.
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6. High-definition spatial transcriptomics visualizes the cellular and molecular architecture underlying perineural invasion in localized prostate cancer.
6. 高清晰度空间转录组学可视化了局限性前列腺癌神经周围侵袭背后的细胞和分子结构PMID:日期:2026-09-01Distinguishing indolent from aggressive tumors remains a key challenge in the clinical management of prostate cancer (PC), highlighting the need for better tools for accurate risk stratification. A defining feature of aggressive PC is its propensity for perineural invasion (PNI), a pathological finding that is associated with poor prognosis. Despite its clinical significance, very little is known about the spatial and molecular determinants of PNI in PC. To address this, we used high-definition spatial transcriptomics (Visium HD) to profile the PNI-associated tumor microenvironment (TME) of a representative PC patient at near single-cell resolution. Spatial mapping of the expressed genes and inferred cell types revealed transcriptionally divergent malignant cell states spatially linked to PNI within this patient. Nerve-invasive PC cells were organized within a distinct spatially localized niche that exhibited altered TME characteristics, including increased proportions of macrophages, CD4 T-cells, and endothelial cells, suggesting coordinated changes in the tumor- and immune microenvironments. The PNI-associated niche in this patient further displayed enrichment of pathways involved in immune regulation and extracellular matrix remodeling, consistent with PNI-associated niche remodeling. APP-CD74 was identified as a potential signaling axis associated with tumor-nerve, nerve-macrophage, and nerve-endothelial cell interactions, suggesting PNI in this patient may be associated with distinct microenvironmental signaling programs. We further revealed a PNI-associated PC signature that held biomarker potential at the early-localized and advanced-metastatic disease stages. Although based on a single patient, these results contribute to our understanding of the spatial and molecular features of PNI in PC and may help guide personalized treatment choices for PC patients in the future.
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7. Mucosal immunity: mechanism and application in cancer immunotherapy.
7. 黏膜免疫：机制及其在癌症免疫治疗中的应用PMID:日期:2026-09-01Recent advances in immunotherapy have significantly revolutionized cancer treatment landscape and prompted extensive research into novel vaccine-based anti-tumor therapy. As the primary defense against external infections, the mucosal immune response plays a pivotal role in maintaining normal physiological functions and preventing pathogen invasion. Mucosal tissues are among the most common sites of tumor initiation, and therefore harnessing mucosal immune to fight against malignant cells represents a feasible option for optimizing and improving current antitumor therapies. Over the past few decades, numerous efforts have been devoted to designing ideal and effective mucosal vaccine. Some clinical trials using mucosal vaccine for cancer therapy have been also launched continually. In this review, we introduce the mechanisms of mucosal immunity, with a focus on the respiratory, gastrointestinal, and urogenital tracts. We also summarize recent research and clinical trials on the application of mucosal vaccines in anti-tumor therapy, aiming to provide new perspectives and directions for future studies.
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8. Glutathione reductase deficiency potentiates the immunogenicity of ferroptosis and cuproptosis via amplified reactive oxygen species accumulation and cGAS-STING pathway activation.
8. 谷胱甘肽还原酶缺乏通过放大的活性氧积累和cGAS-STING通路激活增强铁死亡和铜死亡的免疫原性PMID:日期:2026-09-01Cancer remains a major therapeutic challenge due to drug resistance and metastasis, processes driven by oxidative stress and redox imbalance. Targeting this vulnerability through ferroptosis (iron-dependent lipid peroxidation) and cuproptosis (copper-driven mitochondrial dysfunction), two ROS-mediated cell death pathways, offers a promising therapeutic strategy. However, clinical translation is hindered by incomplete understanding of their redox regulation and limited immunogenicity. A genome-wide CRISPR knockout screen was performed to identify key regulators of ferroptosis. Genetic depletion or pharmacological inhibition of candidate genes was evaluated across multiple cancer cell lines for sensitivity to ferroptosis inducer RSL3 and the cuproptosis inducer elesclomol (Es). Antitumor efficacy was assessed in xenograft, orthotopic, metastatic, and syngeneic mouse models, alone or combined with immune checkpoint inhibitors. Mechanistic studies also examined ROS production, mitochondrial stress, mitochondrial DNA release, cGAS-STING activation, and immune responses within the tumor microenvironment. Glutathione reductase (GSR), a central enzyme maintaining reduced glutathione (GSH) homeostasis, was identified as the top suppressor of ferroptosis. GSR knockout or pharmacological inhibition markedly sensitized diverse cancer cell lines to RSL3-induced ferroptosis, while GSR overexpression conferred resistance. Strikingly, GSR depletion also enhanced sensitivity to cuproptosis triggered by the copper ionophore Es. In multiple in vivo tumor models, GSR inhibition synergizes with RSL3 or Es to suppress tumor growth, inhibit lung metastasis, and prolong survival. Mechanistically, GSR deficiency amplified ROS production, induced mitochondrial stress, and triggered the cytosolic mitochondrial DNA release under ferroptotic or cuproptotic stress, activating the cGAS-STING pathway in vitro and in vivo. This increased inflammatory cytokine production, promoted immunogenic cell death, and enhanced the release of damage-associated molecular patterns (DAMPs), including HMGB1. Together, GSR inhibition combined with a ferroptosis or cuproptosis inducer transformed the tumor microenvironment into a highly immune stimulatory state, thereby enhancing the efficacy of immune checkpoint blockade through increased dendritic cell activation and T-cell infiltration and activation. GSR represents a key molecular node connecting and modulating ferroptosis and cuproptosis through redox regulation. Targeting GSR amplifies ROS-mediated immunogenic cell death, triggers cGAS-STING activation in cancer cells, and enhances the efficacy of cancer immunotherapy, providing a promising redox-based therapeutic strategy.
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9. Current and future therapies for triple-negative breast cancer.
9. 三阴性乳腺癌的当前和未来治疗方法PMID:日期:2026-08-26Triple-negative breast cancer remains an aggressive and biologically heterogeneous breast cancer subtype. Although the therapeutic landscape has expanded, durable disease control remains clinically challenging in many settings. Existing reviews often organize TNBC therapy by drug class or molecular subtype, which can obscure how treatment response is shaped by interacting biological layers. Here, we review current and emerging therapeutic strategies through a three-layer framework: tumor-cell-intrinsic vulnerabilities, the local immune and stromal microenvironment, and host-level systemic modifiers. We summarize established approaches, including chemotherapy, immune checkpoint blockade, antibody-drug conjugates and PARP inhibition in biomarker-defined settings, and distinguish them from maturing or exploratory strategies such as pathway-directed therapy, epigenetic modulation, anti-vascular combinations, regulated cell-death induction, cellular therapy, vaccines, microbiome-related interventions, liquid biopsy, AI-supported multiomics and adaptive trial designs. This framework integrates evidence level, disease stage, biomarker reliability and patient tolerance into treatment selection for TNBC precision therapy.
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10. Plasma biomarkers predicting development of lung cancer 5 years before diagnosis.
10. 血浆生物标志物可在诊断前5年预测肺癌的发生PMID:日期:2026-08-14该文献暂无摘要。