CANCER RESEARCH癌症研究
CANCER RESEARCH(英文缩写 CANCER RES),ISSN 0008-5472,eISSN 1538-7445,中文译名:癌症研究 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 | 13.312 | Q1 |
| 2022 | 11.200 | Q1 |
| 2023 | 12.500 | Q1 |
| 2024 | 16.600 | Q1 |
| 2025 | 22.600 | Q1 |
CANCER RESEARCH 最新收录文献
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1. Longitudinal Surgical Modeling of Early Glioblastoma Recurrence Reveals Emergence of Margin-Associated Neural Programs.
1. 早期胶质母细胞瘤复发的纵向手术建模揭示边缘相关神经程序的出现PMID:日期:2026-10-05Glioblastoma (GBM) is a lethal, treatment-resistant brain cancer characterized by diffuse brain invasion, complex neuron-glioma signaling, and cellular, molecular, and spatial heterogeneity. Surgery is the current mainstay of treatment, aimed at maximizing tumor cytoreduction, decompressing the brain to improve neurological function, and providing material for analyses to inform prognostication and adjuvant treatment selection. To accurately model GBM surgical resection and tissue sampling in preclinical animal models, we developed the Maximal Safe Intracranial Surgery (MSIS) system. MSIS integrated a miniaturized neurosurgical resection device and enabled a safe, tunable, and reproducible approach for intracranial tumor resection, multi-regional biopsy, and longitudinal tissue sampling in murine models, with stereotactic, sterile, and high-viability tissue collection. MSIS was applied across five distinct orthotopic brain tumor models to reproducibly generate histologically and radiologically representative models of post-surgical GBM. Similar to humans, increasing the extent of resection correlated with improved animal survival, and recurrent growth patterns varied significantly by model type. Transcriptional profiles of matched primary vs. post-surgical recurrent tumors revealed enrichment of margin-associated transcriptional states consistent with neuron-glioma signaling. Overall, the MSIS system offers opportunities to model the standard-of-care, dissect the spatial and temporal dynamics of GBM, and pair therapeutic discovery with contextual tumor pathobiology.
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2. Getting comfortable: clonal haematopoiesis creates a senescent niche for expansion.
2. 适应环境：克隆性造血为扩增创造衰老微环境PMID:日期:2026-10-05Clonal haematopoiesis (CH) is characterized by the age-associated expansion of mutant haematopoietic clones. How these clones expand, interact with the niche, and maintain a competitive advantage remains poorly understood. In a recent study published in Nature Cell Biology, Mistry and colleagues uncover that senescence in the bone marrow stromal microenvironment is a key contributor to the clonal growth of haematopoietic stem and progenitor cells (HSPCs) carrying CH mutations. Using mouse models and primary human samples, they show that mutant haematopoietic cells induce MSC senescence through contact-independent, cytokine-mediated signalling involving TNF-α, IL-6 and STAT3. Senescent MSCs preferentially support mutant haematopoietic stem and progenitor cells (HSPCs) over wild-type cells. Moreover, genetic or pharmacological depletion of senescent non-haematopoietic cells reduces CH burden and delays progression towards myeloid neoplasia in mice. By demonstrating that the premalignant niche is actively remodelled to favor mutant haematopoiesis, this study identifies MSC senescence as a relevant mechanism regulating CH evolution and a potential target for early disease intervention.
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3. Aberrant Accumulation of Cyclin D1 Rewires Glutamine Metabolism and Generates a Metabolic Vulnerability in Squamous Cell Carcinoma.
3. Cyclin D1的异常积累重编程谷氨酰胺代谢并在鳞状细胞癌中产生代谢脆弱性PMID:日期:2026-10-05Excessive cyclin D1 accumulation is a frequent oncogenic event in head and neck squamous cell carcinoma (HNSCC) and esophageal squamous cell carcinoma (ESCC). Although classically associated with enhanced proliferation and genomic instability, we revealed that cyclin D1 dysregulation induces metabolic rewiring that leads to unexpected metabolic dependencies. Sustained nuclear retention of cyclin D1 drove metabolic reprogramming through activation of CDK4/6 and downregulation of mitochondrial isocitrate dehydrogenase 3 (IDH3), reducing α-ketoglutarate and NADH production. This metabolic alteration increased glutamine dependence and elevated autophagic flux, and co-targeting autophagy and glutamine metabolism suppressed the growth of squamous cell carcinoma models in vitro and in vivo. Together, these findings highlight a therapeutic strategy for HNSCC and ESCC that leverages metabolic reprogramming induced by dysregulated cyclin D1/CDK4 activity, with potential applicability to patients with tumors refractory to conventional therapies.
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4. Stromal MTHFD2 Links Fibrotic Remodeling to Immune Evasion via Redox-Dependent Inflammatory Signaling in Lung Adenocarcinoma.
4. 基质MTHFD2通过氧化还原依赖性炎症信号将肺腺癌的纤维化重塑与免疫逃逸相关联PMID:日期:2026-10-05Fibroblast activation and extracellular matrix stiffening are hallmarks of the fibrotic tumor microenvironment. Fibrotic microenvironmental remodeling is also linked to immune exclusion and evasion, suggesting that common microenvironmental signals might coordinate both fibrotic and inflammatory outputs. Here, we identified methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) as a redox-sensitive metabolic regulator linking TGF-β-driven fibroblast activation to inflammatory signaling in lung adenocarcinoma (LUAD). MTHFD2 was elevated in cancer-associated fibroblasts across multiple scRNA-seq datasets, and TGF-β induced MTHFD2 even under compliant matrix conditions, with matrix stiffening further enhancing its expression. Notably, while MTHFD2 knockdown suppressed both myofibroblastic and inflammatory programs, enforced expression was sufficient to drive inflammatory cytokine production even in the absence of TGF-β, and this response was further amplified by concomitant TGF-β signaling. These MTHFD2-mediated responses depended on redox perturbation rather than biosynthetic one-carbon metabolism, as they resisted formate supplementation but responded to pro-oxidants. Mechanistically, MTHFD2-driven redox imbalance promoted mitochondrial stress, cytosolic mitochondrial DNA accumulation, and activation of the cGAS-STING-NF-κB pathway, resulting in IL-6 and IL-8 production. Fibroblast-specific MTHFD2 knockdown suppressed paracrine PD-L1 induction in tumor cells and inhibited tumor growth in vivo in an immune-dependent manner. Clinically, high stromal MTHFD2 correlated with epithelial PD-L1 expression and poor LUAD prognosis. Together, these findings identify stromal MTHFD2 as a redox-sensitive metabolic checkpoint linking fibrotic remodeling to immune evasion.
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5. Placenta-Related PEG10 Inhibits mRNA Decay to Promote Glucose Metabolism and Tumor Progression in Hepatocellular Carcinoma.
5. 胎盘相关的PEG10抑制mRNA降解，促进肝细胞癌中的葡萄糖代谢和肿瘤进展PMID:日期:2026-10-02Tumors display marked similarities with embryos, exploiting embryonic developmental programs. Beyond the embryo, the placenta also shares features with malignant tumors, such as invasion, immune evasion, and rapid nutrient exchange, highlighting the need for mechanistic investigations of tumor development through the lens of placental biology. In this study, by screening placental-specific genes with aberrant expression in hepatocellular carcinoma (HCC), we found that the paternally expressed gene 10 (PEG10, a retrovirus-like gene) was overexpressed in HCC and associated with poor patient prognosis. Liver-specific deletion of Peg10 significantly impeded hepatocarcinogenesis and tumor progression in a hydrodynamic tail vein injection-induced HCC mouse model. PEG10 drove tumor cells to co-opt the metabolic phenotype of trophoblast cells by upregulating key glucose metabolic regulators glucose transporter 1 (GLUT1) and hexokinase 2 (HK2). Mechanistically, as an RNA-binding protein (RBP), PEG10 inhibited the Staufen1-mediated mRNA decay (SMD) pathway, stabilizing GLUT1 and HK2 mRNA to enhance glucose uptake and aerobic glycolysis. Furthermore, retinoic acid pharmacologically suppressed PEG10 expression, effectively abrogating the adaptive metabolic advantage and acting synergistically with sorafenib to restrict tumor growth. Collectively, this study reveals how HCC aberrantly reactivates the placental gene PEG10 to orchestrate oncogenic glucose uptake and metabolism, identifying it as a compelling therapeutic target for metabolic intervention in cancer.
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6. ScanTCR Enables Early Cancer Detection by Repertoire-Scale Representation of Cancer-Associated T-Cell Receptors in Peripheral Blood.
6. ScanTCR通过外周血中癌症相关T细胞受体的库尺度表征实现早期癌症检测PMID:日期:2026-10-02T cells initiate anticancer immune responses at an early stage of tumorigenesis, thus enabling dynamic monitoring of peripheral blood T-cell receptor (TCR) repertoire changes as a promising strategy for early cancer detection. However, current TCR-based cancer detection methods focus on limited high-frequency TCRs instead of repertoire-scale representation, overlooking numerous crucial cancer-associated TCRs (caTCRs). Herein, we developed ScanTCR, a computational framework for early cancer detection that introduces a reference-guided repertoire-scale encoding method capable of incorporating all TCRs. ScanTCR exhibited remarkable precision in distinguishing cancer patients from non-cancer individuals using peripheral blood TCR. In a pan-cancer analysis encompassing seven cancer types, ScanTCR demonstrated robust performance in detecting both cancer types included in the training data and unseen cancer types, surpassing state-of-the-art TCR-based methods. Furthermore, ScanTCR identified caTCRs whose corresponding T cells exhibit enhanced cellular immune capacity. Collectively, this work proposes a TCR-based approach enabling repertoire-scale representation of immune receptors for noninvasive early cancer detection.
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7. EZH2 Inhibition Induces a Metabolic Stress Response Sensitizing Triple-Negative Breast Cancer to Glutaminase Targeting.
7. EZH2抑制诱导代谢应激反应，使三阴性乳腺癌对谷氨酰胺酶靶向治疗敏感PMID:日期:2026-10-02EZH2, the catalytic subunit of the histone methyltransferase complex PRC2, is overexpressed and associated with poor prognosis in triple-negative breast cancer (TNBC). Although EZH2 inhibition significantly alters chromatin landscapes and gene expression, it has limited impact on the growth of TNBC models, suggesting adaptive compensatory mechanisms. Here, we demonstrated that EZH2 inhibition causes the accumulation of misfolded proteins and double-stranded RNA (dsRNA), triggering an essential integrated stress response (ISR) through PKR and PERK activation. By inducing ISR-mediated ATF4, EZH2 inhibition enhanced amino acid flux and promoted glutaminolysis to support TNBC cell survival. Pharmacological targeting of this metabolic axis with a glutaminase inhibitor in combination with EZH2 inhibition significantly impaired TNBC cell proliferation and tumor growth. These findings reveal a stress-driven metabolic adaptation that sustains TNBC survival upon EZH2 blockade and highlight inhibition of this pathway as a strategy to enhance the efficacy of EZH2 inhibitors in TNBC.
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8. Targeting Distinct Cell Cycle Nodes Overcomes RAS Inhibitor Resistance.
8. 靶向不同的细胞周期节点克服RAS抑制剂耐药性PMID:日期:2026-10-02Activating mutations in KRAS drive pancreatic ductal adenocarcinoma (PDAC) and non-small cell lung cancer (NSCLC). Although mutant-selective KRAS inhibitors and pan-RAS inhibitors provide clinical benefits, the development of resistance limits durable responses. Here, transcriptomic and proteomic analyses revealed that, despite effective suppression of mutant KRAS signaling, resistant cells sustain cell cycle progression. Distinct orthogonal mitogenic pathways were engaged in a context-dependent manner to bypass KRAS inhibition. While these pathways could be broadly inhibited using the pan-RAS-ON inhibitor RMC-6236, cells remained capable of developing acquired resistance where cell proliferation was uncoupled from RAS signaling. Combinatorial drug screens and genome-wide CRISPR-Cas9 screens showed that perturbing cell cycle nodes via targeting cyclin dependent kinases CDK4/6 and CDK2 restored sensitivity to KRAS/RAS inhibitors. Co-targeting CDK4/6 induced G1 arrest and suppressed E2F-regulated proteins across all resistant models. In contrast, co-targeting CDK2 exerted a broader effect by impairing DNA replication, inducing G2 arrest, preventing mitotic entry, and yielding a more durable cytostatic response that delayed cellular outgrowth after drug withdrawal. Finally, concurrent inhibition of KRAS with either CDK4/6 or CDK2 yielded durable tumor control in vivo in xenografts derived from models with acquired resistance. In conclusion, these findings identify sustained cell cycle activity as a defining feature of resistance to KRAS-directed therapies and establish cell cycle co-targeting as an effective strategy to overcome KRAS/RAS inhibitor resistance.
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9. MYC-Dependent rRNA Catabolism Stress Dictates Survival Heterogeneity of Hepatocellular Carcinoma Cells Under Glutamine Deprivation.
9. MYC依赖的rRNA分解代谢应激决定肝细胞癌细胞在谷氨酰胺剥夺下的生存异质性PMID:日期:2026-09-29Tumor cells commonly exhibit a preferential uptake of glutamine to support the heightened metabolic demands. However, the therapeutic potential of targeting glutamine metabolism is severely limited by the heterogeneous responses of cancer cells to glutamine deprivation. In this study, we identified a ribophagy-adenosine-MYC positive feedback loop that was activated and determined cell fate under glutamine deprivation. In sensitive cells, highly expressed MYC acted as a scaffold to recruit Unc-51 like autophagy activating kinase 1, which phosphorylated ribosomal protein L12 to initiate ribophagy. This process drove extensive rRNA catabolism and a burst of reactive oxygen species, ultimately leading to cell death. Moreover, adenosine generated during this cascade enhanced MYC expression via its 3'-UTR region, locking the loop into a self-reinforcing hyperactivated state. In contrast, tolerant cells exhibited lower MYC expression, which constrained the loop to a low-activity and subcritical steady state, thereby enabling survival under glutamine deprivation. Consequently, MYC-high tumors were vulnerable to glutaminase inhibition alone (CB-839), while MYC-low tumors required combination therapy with CB-839 and a pro-oxidant (elesclomol) to achieve tumor eradication. This study establishes MYC expression as a key determinant of sensitivity to glutamine deprivation, reveals the central role of ribophagy within the glutamine deprivation-triggered positive feedback loop, and uncovers a non-canonical, scaffold-like function of MYC in rRNA catabolism. These findings highlight a potential combination strategy to overcome a major bottleneck in targeting glutamine metabolism.
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10. Spatial Analysis Dissects the Microenvironmental Architecture of Local Recurrence after Breast-Conserving Surgery.
10. 空间分析解析保乳术后局部复发的微环境结构PMID:日期:2026-09-25Ipsilateral breast tumor recurrence (IBTR) is a critical prognostic determinant in breast cancer patients undergoing breast-conserving surgery (BCS). The spatial arrangement of immune, stromal, and malignant cells can influence local recurrence progression and treatment efficacy in IBTR tumors. Here, we performed single-cell spatial transcriptomics on primary breast cancer (PBC) and matched IBTR specimens from 22 patients, comprising 18 true recurrence (TR) and 4 new primary (NP) cases, to generate a comprehensive atlas of over 600,000 cells. Cellular neighborhood (CN) analysis identified a specific tumor cell-stromal region significantly enriched in IBTR tumors. Tumor recurrence was driven by a highly proliferative epithelial cell subpopulation characterized by immune exclusion and invasive features. Spatial analysis uncovered a tumor-stromal region where CD24+ tumor cells spatially intersected with BGN+ cancer-associated fibroblasts (CAFs) alongside upregulation of MDK signaling. In parallel, the BGN+ CAFs displayed enriched CXCL12 pathways, suggesting a potential spatial axis that aligns with local immunosuppressive remodeling and recurrent niche formation. Critically, the spatial colocalization of CD24⁺ tumor cells and BGN⁺ CAFs was validated as an independent predictor of recurrence after BCS. This study delivers a high-resolution spatial landscape of IBTR, uncovering distinct microenvironmental landscapes between TR and NP subtypes, and establishes these spatially defined cellular networks as both mechanistic drivers and translatable prognostic biomarkers.