CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY肿瘤学与血液学评论
CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY(英文缩写 CRIT REV ONCOL HEMAT),ISSN 1040-8428,eISSN 1879-0461,中文译名:肿瘤学与血液学评论 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
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 6.625 | Q1 |
| 2022 | 6.200 | Q1 |
| 2023 | 5.500 | Q1 |
| 2024 | 5.600 | Q1 |
| 2025 | 6.200 | Q1 |
CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY 最新收录文献
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1. Immunosenescence in tumor progression: from synergistic mechanisms to therapeutic strategies.
1. 肿瘤进展中的免疫衰老：从协同机制到治疗策略PMID:日期:2026-10-03Tumor-associated immunosenescence is not a decline in immune function, but rather a state of immune ecological imbalance. It drives tumor progression through multi-dimensional mechanisms, including decreased immune surveillance, chronic inflammation, accumulation of suppressive cells, remodeling of TME, metabolic disorders, and epigenetic regulation. The challenges in immunosenescence research include conceptual confusion, an imbalance in research perspectives, the limitations of preclinical models, and the translational hurdles. This review summarizes the latest research findings on the role of immunosenescence in tumor progression and its multiple regulatory mechanisms and highlights the promise of targeted therapeutic strategies against immunosenescence. The synergy among multiple mechanisms of immunosenescence creates a self-reinforcing cycle of chronic inflammation and immune dysfunction, thereby driving immune ecological imbalance. The core strategies of targeted therapy for immunosenescence include eliminating or regulating senescent immune cells to rejuvenate the immune system, as well as enhancing the immune system's ability to clear senescent cells, thereby achieving immune ecosystem remodeling. Future research should focus on deciphering the deep heterogeneity of immunosenescence, elucidating the mechanisms of key overlapping processes such as T-cell exhaustion, developing clinical tools for precise assessment of immune age, optimizing preclinical models, and conducting innovative "immune age-oriented" clinical trials.
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2. Conformational switching and spatial heterogeneity: Decoding SERPINE1/PAI-1as a multifaceted driver of tumor progression and therapy resistance.
2. 构象转换与空间异质性：解读SERPINE1/PAI-1作为肿瘤进展和治疗耐药的多层面驱动因素PMID:日期:2026-10-02Plasminogen activator inhibitor-1 (PAI-1), a central fibrinolytic regulator encoded by the SERPINE1 gene, is increasingly recognized as a context-dependent molecular hub in tumor biology. Despite its canonical protease-inhibitory role, elevated PAI-1 levels are associated with metastasis and poor prognosis in many malignancies, creating an apparent functional paradox. This review examines how reactive-center-loop conformational transitions, binding partners, cellular source, and anatomical compartment can alter SERPINE1 output. We compare tissue-specific circuits across lung, breast, colorectal, and neural tumors and incorporate recent evidence that SERPINE1 loss can engage distinct p53/SMAD3-MCM3, uPAR-ERK/p38, and HSP90α-p38-MMP-1 modules. We also evaluate a testable convergence model linking GDNF-GFRα1-RET signaling to SERPINE1 regulation and downstream PAI-1-associated pathways in neural tumors, while emphasizing that a direct causal connection has not yet been demonstrated. Finally, we frame the concentration-dependent inflammation-invasion switch as a working hypothesis and assess therapeutic strategies, including TM5614 and ACT001, in relation to tumor context and hemostatic safety.
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3. Mechanistic Role of eIF4E in the Hallmarks of Cancer: A Translational Control Perspective.
PMID:日期:2026-10-02Cancer progression is driven by coordinated dysregulation of signaling and gene-expression programs that sustain multiple hallmarks of malignancy. Eukaryotic initiation factor 4E (eIF4E) has emerged as an important determinant of this translational reprogramming by preferentially enhancing the synthesis of proteins that support oncogenic phenotypes. This review critically examines the mechanistic evidence linking eIF4E-dependent translation to major cancer hallmarks, including sustained proliferative signaling, evasion of apoptosis, tumor-promoting inflammation, angiogenesis, invasion, and metastasis. We discuss how dysregulated eIF4E activity, driven in part by the PI3K/AKT/mTOR and MAPK/MNK pathways, promotes selective translation of oncogenic, survival, stress-response, hypoxia-, and epithelial-mesenchymal transition-associated factors. We further examine evidence implicating eIF4E in the regulation of p53- and telomerase reverse transcriptase (TERT)-dependent pathways, highlighting potential links to genomic instability and replicative immortality. Finally, we evaluate pharmacological strategies targeting eIF4E and discuss the opportunities and challenges of exploiting eIF4E-dependent translational and metabolic vulnerabilities for cancer therapy. Collectively, the evidence supports eIF4E as a therapeutically relevant translational regulator whose functional activity, rather than expression alone, may help define tumor dependencies and inform mechanism-based therapeutic strategies.
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4. Abundance is not survival: intratumoural immune-cell fate as a missing endpoint in antibody-drug conjugate and checkpoint blockade combinations for triple-negative breast cancer.
4. 丰度不等于生存：瘤内免疫细胞命运是抗体药物偶联物与检查点阻断联合治疗三阴性乳腺癌中缺失的终点PMID:日期:2026-09-29Antibody-drug conjugates (ADCs) have reshaped metastatic triple-negative breast cancer, and combining them with checkpoint inhibitors is close to consensus: cytotoxic payloads kill tumour cells in ways that release antigen and expose damage-associated signals. We argue that a specific endpoint is missing from both sides of the question. Preclinical ADC studies report the abundance and activation phenotype of intratumoural immune populations, not their survival, and that reflects endpoint convention, not technical limitation. Payload diffusion is governed by the physical chemistry of the released molecule and the geometry of the tissue it crosses, not by the identity of the cell it reaches; the dendritic cells and lymphocytes on which checkpoint blockade depends occupy the same space. Only three randomised breast cancer datasets permit interpretation, none is powered to isolate the checkpoint contribution, and predictive biomarkers have not performed. We examine payload distribution in tissue, immune-population exposure and susceptibility, the consequences of payload class, and the lymphodepletion, corticosteroid and growth-factor exposures that trial protocols impose. Evidence is graded as direct, indirect, inferred or not measured, and it runs both ways: antigen-independent uptake is documented, yet microtubule payloads mature intratumoural dendritic cells and auristatin conjugates against 4-1BB failed to deplete activated T cells at any drug-to-antibody ratio tested. Intratumoural immune-cell fate is therefore an unmeasured variable rather than a demonstrated cause, and three propositions treated as settled mechanism should be restated as hypotheses. Resolving them requires matched-linker conjugates, spatially resolved survival endpoints, and covariates that trials can analyse retrospectively.
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5. Reporting inconsistencies in a meta-analysis of sarcopenia and the prognostic nutritional index in immune checkpoint inhibitor-treated head and neck cancer.
5. 关于肌少症与预后营养指数在免疫检查点抑制剂治疗的 head and neck cancer 中的荟萃分析报告不一致性PMID:日期:2026-09-29该文献暂无摘要。
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6. Clinical Implications of the Type and Genomic Location of Pathogenic BRCA1 and BRCA2 Variants in Hereditary Breast and Ovarian Cancer.
6. 遗传性乳腺癌和卵巢癌中致病性BRCA1和BRCA2变异类型及基因组位置的临床意义PMID:日期:2026-09-29Germline pathogenic or likely pathogenic variants (P/LPVs) in BRCA1 and BRCA2 are major determinants of hereditary breast and ovarian cancer susceptibility. Although clinical management has traditionally relied on the presence of a BRCA1/BRCA2 alteration regardless of its specific characteristics, growing evidence suggests that not all BRCA P/LPVs are biologically and clinically equivalent. Variant location within BRCA1 and BRCA2 influences the relative distribution of breast and ovarian cancer risk. Breast cancer cluster regions (BCCRs) are associated with a higher relative risk of breast versus ovarian cancer, whereas ovarian cancer cluster regions (OCCRs), largely encompassing exon 11, are associated with a relative shift toward ovarian cancer risk. Variant type may also be clinically relevant. Protein-truncating P/LPVs have been associated with higher cancer risks than selected missense variants with residual protein function and lower penetrance. Some studies have also reported poorer outcomes for carriers of protein-truncating P/LPVs and more favorable outcomes for those with missense variants. In this narrative review, we summarize current evidence on the clinical implications of BRCA1/BRCA2 P/LPV type and genomic location. While associations between variant location and breast or ovarian cancer risk are supported by large international consortia, prognostic and predictive associations remain largely exploratory. A better understanding of variant-specific genotype-phenotype correlations may ultimately refine risk prediction, preventive strategies, and treatment selection in hereditary breast and ovarian cancer.
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7. Mechanical immune checkpoints in tumors: Mechanosensing, immunosuppressive networks, and therapeutic modulation.
7. 肿瘤中的机械免疫检查点：机械感知、免疫抑制网络与治疗性调控PMID:日期:2026-09-28Solid tumors undergo significant biomechanical remodeling, which includes ECM stiffening, collagen crosslinking and alignment, increased interstitial fluid pressure, solid stress, vascular compression, and altered viscoelastic properties. These biomechanical abnormalities function not merely as passive structural features but actively influence tumor progression and immune evasion. Emerging evidence introduces the concept of mechanical immune checkpoints, defined as mechanosensory immunoregulatory circuits that link specific biomechanical signals to impaired antitumor immunity through identifiable mechanosensory or mechanotransduction pathways This review first summarizes the mechanisms through which aberrant tumor mechanics contribute to T-cell exclusion, T-cell exhaustion, suppressive myeloid differentiation, and stromal remodeling. Subsequently, it discusses therapeutic strategies, including ECM remodeling, inhibition of mechanotransduction, modulation of mechanosensors and tumor cell stiffness, as well as rational combinations with traditional immune checkpoint blockade. Lastly, the translational maturity of current strategies is critically assessed, highlighting priorities for biomarker-guided combination therapy. By conceptualizing force-sensitive immunosuppressive circuits within a clinically relevant framework, mechanical immune checkpoints may facilitate biomarker-guided patient stratification and rational combination approaches to enhance immunotherapy efficacy in mechanically resistant solid tumors.
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8. Menin inhibitors in acute myeloid leukaemia: Mechanisms, clinical pharmacology, and emerging therapeutic strategies.
8. 急性髓系白血病中的Menin抑制剂：机制、临床药理学及新兴治疗策略PMID:日期:2026-09-28Acute myeloid leukaemia (AML) remains associated with poor outcomes in relapsed or refractory disease and in molecularly defined high-risk subgroups. AML with KMT2A rearrangements (KMT2Ar) or NPM1 mutations (NPM1m) shares a dependence on the menin-KMT2A interaction, which sustains HOXA/MEIS1-driven transcription required for leukaemic maintenance. This dependence has provided the rationale for developing menin inhibitors as a targeted approach in selected AML subsets. This review summarises the mechanistic basis, clinical pharmacology, and current clinical role of menin inhibitors in AML. Revumenib, ziftomenib, bleximenib, and enzomenib are orally administered small molecules that disrupt menin-dependent transcription, induce myeloid differentiation, and have shown clinical activity in KMT2Ar and NPM1m AML. Monotherapy has produced clinically relevant remission rates in relapsed or refractory disease, and early-phase combinations with venetoclax-based therapy, hypomethylating agents, intensive chemotherapy, or FLT3 inhibitors have shown higher response rates in selected settings. Despite sharing a common target, these agents differ in dosing schedule, pharmacokinetic profile, CYP3A4-mediated drug-drug interaction potential, sensitivity to food or gastric pH, and safety profile. Differentiation syndrome and QTc prolongation are the principal toxicities requiring monitoring, although QT liability appears to vary across compounds. Acquired resistance-mediated by MEN1 binding-pocket mutations, co-occurring genomic alterations, and adaptive transcriptional or epigenetic programmes-remains a clinical limitation. Current evidence supports menin inhibition as a targeted strategy for molecularly selected AML. Ongoing studies will be important for defining optimal sequencing, combination regimens, approaches to resistance, and the role of pharmacologically informed dose optimisation in routine practice.
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9. Tumor-infiltrating B cells in cancer immunity: Heterogeneity, spatial organization, and context-dependent function.
PMID:日期:2026-09-28Tumor-infiltrating B cells are emerging as critical regulators of cancer immunity. Recent single-cell and spatial studies have shown that their functions extend beyond antibody production to include antigen presentation, tertiary lymphoid structure (TLS) organization, T cell modulation, cytokine-mediated regulation, and myeloid crosstalk. However, the clinical and immunological roles of B cells in cancer are highly context-dependent. In some tumors, B cell infiltration, particularly within mature TLSs, is associated with improved survival and enhanced responses to immune checkpoint blockade. In other settings, regulatory B cells or immunosuppressive plasma cells can promote tumor progression by suppressing cytotoxic lymphocytes, reinforcing regulatory immune networks, or cooperating with suppressive myeloid populations. These divergent observations indicate that B cells should not be interpreted as uniformly anti-tumor or pro-tumor. Instead, their functions are shaped by developmental state, spatial localization, inflammatory cues, antigenic specificity, and cellular interaction networks. In this review, we discuss tumor-infiltrating B cells through a context-dependent framework. We propose that B cells support anti-tumor immunity when integrated into organized lymphoid niches and engaged in productive T cell-B cell cooperation, whereas they promote immune escape when redirected toward regulatory programs or suppressive myeloid interactions. Understanding this functional plasticity may help reconcile differences across cancer types and guide the development of B cell-informed biomarkers and therapeutic strategies.
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10. Reassessing the clinical value of momelotinib in myelofibrosis: An ESMO-MCBS:H-based appraisal of SIMPLIFY-1 and MOMENTUM.
PMID:日期:2026-09-26Myelofibrosis (MF) is a chronic myeloproliferative neoplasm characterized by splenomegaly, systemic symptoms, and anemia, the latter being strongly associated with poor survival and reduced quality of life. Current Janus kinase (JAK) inhibitors improve symptoms and spleen size but often exacerbate anemia, leaving a significant unmet clinical need. Momelotinib, a JAK1/JAK2 and activin A receptor type 1 (ACVR1) inhibitor, has been proposed to address both splenomegaly and anemia through hepcidin suppression. This study critically evaluates the clinical benefit of momelotinib using the European Society for Medical Oncology Magnitude of Clinical Benefit Scale for Hematological Malignancies (ESMO-MCBS:H), focusing on the phase 3 trials SIMPLIFY-1 and MOMENTUM. In SIMPLIFY-1, momelotinib demonstrated non-inferiority to ruxolitinib in terms of spleen volume reduction (SVR35 26.5% vs 29.0%) and did not evaluated quality of life as a prespecified outcome, resulting in an ESMO-MCBS:H score indicating no evaluable benefit (NEB). In contrast, in MOMENTUM, conducted in symptomatic, anemic patients previously treated with JAK inhibitors, momelotinib was superior to danazol for MFSAF total symptom score response (≥50% reduction from baseline 25% vs 9%). As no improvement in global health status was observed, MOMENTUM was scored as Grade 1. Interpretation of hematologic benefits remains limited by trial design, as the anemia related outcomes were not primary endpoints and studies were not powered to robustly assess them. Furthermore, the negative SIMPLIFY-2 trial underscores uncertainty in pretreated populations. In conclusion, momelotinib demonstrates a differentiated clinical profile with consistent spleen control and potential hematologic benefits, particularly in anemic patients. However, superiority over other improved JAK inhibitors has not been demonstrated in the pivotal phase 3 trials evaluated. Future trials incorporating anemia-focused primary endpoints and biomarker stratification are warranted to better define its role in myelofibrosis management.