Cancer Biology & Medicine癌症生物学与医学
Cancer Biology & Medicine(英文缩写 CANCER BIOL MED),ISSN 2095-3941,eISSN 2095-3941,中文译名:癌症生物学与医学 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 | 5.347 | Q2 |
| 2022 | 5.500 | Q2 |
| 2023 | 5.600 | Q1 |
| 2024 | 8.400 | Q1 |
| 2025 | 12.400 | Q1 |
Cancer Biology & Medicine 最新收录文献
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1. Efbemalenograstim alfa as prophylaxis for chemotherapy-induced neutropenia in patients with non-small-cell lung cancer: a randomized, multicenter, phase II trial.
PMID:日期:2026-09-17Primary prophylaxis with granulocyte colony-stimulating factor (G-CSF) is recommended for patients receiving chemotherapy with a high risk of febrile neutropenia (FN), but its use remains suboptimal in patients receiving intermediate-risk regimens who have additional risk factors, for whom secondary prophylaxis (SPx) is commonly used despite limited prospective evidence comparing the two approaches. This study evaluated efbemalenograstim alfa (EFBGα), a novel Fc fusion G-CSF, as primary or secondary prophylaxis for chemotherapy-induced neutropenia (CIN) in patients with non-small-cell lung cancer (NSCLC) receiving intermediate-risk FN regimens who have additional risk factors. This multicenter, randomized phase II trial enrolled chemotherapy-naïve patients with stage IIIB/IV NSCLC scheduled for platinum-taxane chemotherapy. Patients were randomized 2:1 to either primary prophylaxis (EFBGα 20 mg at 48 ± 4 h after each cycle) or secondary prophylaxis (given only after grade 3-4 neutropenia). The primary endpoint was the cycle 1 incidence of grade 3-4 neutropenia. A total of 102 patients were enrolled between February 2024 and December 2025, of whom 96 were included in the analysis: 63 in the primary prophylaxis group and 33 in the secondary prophylaxis group. In cycle 1, the incidence of grade 3-4 neutropenia was lower with primary prophylaxis than with secondary prophylaxis [20.6%, 95% confidence interval (CI) 11.5%-32.7% 57.6%, 95% CI 39.2%-74.5%; risk difference -36.9%, 95% CI -52.4% to -16.1%; < 0.001]. The median duration of grade 3-4 neutropenia was comparable between the groups ( = 0.144). Cycle 1 FN incidence was 1.6% in the primary and 6.1% in the secondary prophylaxis group. Treatment-related adverse events were mostly grade 1-2, with pain-related events (7.0%) being the most common. EFBGα exhibited promising efficacy and tolerability for CIN prophylaxis in patients with NSCLC and additional risk factors who are receiving intermediate-risk chemotherapy (IRC). The results support its use in both primary and secondary prophylactic strategies, and earlier initiation was associated with better CIN control.
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2. Revisiting the immunosuppressive microenvironment in hepatocellular carcinoma: a functional taxonomy of immune cells and therapeutic targeting.
PMID:日期:2026-09-15Despite transformative success in other solid tumors, immunotherapy has encountered a formidable barrier in hepatocellular carcinoma (HCC), a profoundly immunosuppressive tumor microenvironment (TME) that is predominantly "cold" and also exhibits remarkable heterogeneity across patients. This inter-patient variability in the immune context leads to different responses to treatment, limits clinical efficacy, and highlights the critical need for a deeper, systems-level understanding of the HCC immune landscape. This review provides an integrated and conceptual analysis of the HCC immune landscape. It delineates the mechanistic drivers underlying immune suppression, summarizes current immune-based classification frameworks, and dissects the context-dependent functions of key immune cell populations in tumor progression. Furthermore, this review surveys established TME-targeting therapies comprising primarily immune checkpoint blockade strategies and their clinically validated combinations, and highlights emerging agents and concepts under preclinical and early clinical development. By integrating mechanistic insights with immune classification and therapeutic advances, this review aims to provide a unifying framework to inform the rational design of next-generation immunotherapies for HCC.
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3. Migrasome-propagated ITGβ3-TGFβ1 circuit orchestrates breast cancer brain metastasis by reprogramming the microglial niche.
PMID:日期:2026-09-08The dismal prognosis of breast cancer brain metastasis (BCBM) is attributed to a maladapted tumor microenvironment. This study was aimed at deciphering the role of novel intercellular communicators, tumor-derived migrasomes, in driving BCBM progression, with a focus on their ability to co-opt brain-resident microglia. Migrasomes were isolated and characterized from brain-tropic (231-BR; Mig-BCBM) and parental breast cancer cells, patient-derived metastatic breast cancer tissues, and mice BCBM tissues. The functional axis was delineated through an integrative approach encompassing proteomics, co-culture systems, brain colonization assays, genetic perturbations, and a pharmacological intervention with the clinical-stage TGFβR1 inhibitor galunisertib. Mig-BCBM were internalized by microglia, thus triggering their repolarization to a pro-tumorigenic, M2-like state, both and . Proteomic profiling identified integrin β3 (ITGβ3) as a key regulator selectively packaged into Mig-BCBM. Mechanistically, migrasomal ITGβ3 activated the PI3K/AKT pathway in microglia, thus driving M2 polarization. These reprogrammed microglia secreted high levels of TGFβ1, which in turn fostered a metastatic niche by inducing Smad2/3-dependent epithelial-mesenchymal transition (EMT) in tumor cells. Crucially, we uncovered a self-amplifying feedforward loop in which microglial-derived TGFβ1 transcriptionally upregulates TSPAN4 EGR1 in cancer cells, thus enhancing migrasome biogenesis and subsequent ITGβ3 loading. Disrupting this loop with galunisertib potently inhibited BCBM outgrowth and colonization , without systemic toxicity. This study identified a targetable circuit in BCBM wherein tumor-derived migrasomes, ITGβ3, engage microglia in a TGFβ1-centered crosstalk. Because this self-reinforcing ITGβ3-TGFβ1 axis sustains the pro-metastatic niche, its disruption might provide a rational therapeutic strategy.
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4. Erratum to From residual risk to precision intervention: the evolving role of minimal residual disease in breast cancer management.
4. 勘误：从残余风险到精准干预——微小残留病灶在乳腺癌管理中不断演变的作用PMID:日期:2026-09-08该文献暂无摘要。
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5. cGAS-STING pathway activation drives the cold-to-hot tumor transition and sensitizes immunotherapy.
PMID:日期:2026-08-13The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway is a central sensor of innate immunity that plays critical roles in recognizing cytosolic DNA and initiating antitumor immune responses. However, this pathway exhibits extensive spatiotemporal duality and context dependency in tumor regulation. In recent years, modulating this pathway to convert immunologically "cold" tumors into immunologically "hot," inflamed tumors has emerged as a cutting-edge strategy to reverse resistance to immune checkpoint inhibitors (ICIs). This review outlines the molecular mechanisms underlying the activation and regulation of the cGAS-STING pathway, with emphasis on its complex role in orchestrating the tumor immune phenotypic switch. A nuanced analysis of the pathway's duality distinguishes between acute immunostimulatory activation and chronic, pro-tumorigenic inflammation driven by chromosomal instability (CIN). Furthermore, current evidence regarding direct and indirect T-cell modulation, as well as pathway-mediated remodeling of the tumor microenvironment (TME) across diverse malignancies, is discussed in detail. Crucially, the current bottlenecks in clinical translation are described, including evaluation of the failure of first-generation agonists and the promise of next-generation delivery platforms such as antibody-drug conjugates (ADCs) and nanoparticle systems. Finally, a novel strategic framework is proposed involving mapping of specific STING-targeted modalities to distinct TME phenotypes, such as immune-desert, immune-excluded, and exhausted-inflamed states. A detailed understanding of the cGAS-STING axis has substantial value in providing theoretical guidance and supporting clinical translation in the development of next-generation combination immunotherapies, as well as broadening the patient population benefiting from clinical interventions.
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7. Global landscape and temporal trends in lifetime risk of colorectal cancer in 185 countries: a population-based study.
PMID:日期:2026-08-06Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer-related mortality worldwide. This study was aimed at estimating regional and national variations in lifetime CRC risk worldwide. CRC data were extracted from GLOBOCAN 2022, including 185 countries, and population and all-cause mortality data were sourced from the United Nations. The world was divided into 20 geographical regions and categorized by Human Development Index (HDI). Lifetime CRC risk was estimated with the life table method, adjusted for multiple primary cancers. In 2022, the lifetime risks of developing and dying from CRC were 2.69% [95% confidence interval (CI): 2.68-2.70] and 1.39% (95% CI: 1.39-1.40), respectively. Men had a higher risk of colon cancer than rectal cancer, and higher CRC risk than women. Lifetime risk varied by region and HDI: regions with very high, high, moderate, and low HDI had incidence risks of 5.17%, 2.75%, 0.72%, and 0.57%, respectively, and mortality risks of 2.48%, 1.50%, 0.44%, and 0.41%, respectively. Australia/New Zealand had the highest incidence risk (7.41%, 95% CI: 7.30-7.52), and Northern Europe the highest mortality risk (3.28%, 95% CI: 3.24-3.32). Risks were stable before 40 years of age, peaked in middle age, and declined after 70 years of age. Temporally, Thailand had the highest increasing trend in lifetime risk, whereas the United States and Austria showed a decreasing trend. Lifetime CRC risk differs by subtype, sex, HDI, and geography, and residual risk gradually decreases with age. Targeted primary prevention strategies should be implemented in various countries and regions to mitigate CRC burden.
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8. Anogenital human papillomavirus infection patterns by anatomical site and sexual orientation in Chinese men: a national multi-center study.
8. 中国男性肛门生殖器人乳头瘤病毒感染模式按解剖部位和性取向分析：一项全国多中心研究PMID:日期:2026-08-04该文献暂无摘要。
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9. FDX1 expression promotes DSF/Cu-induced cuproptosis in gastric cancer cells.
9. FDX1表达促进DSF/Cu诱导的胃癌细胞铜死亡PMID:日期:2026-07-28[中文摘要] 胃癌（GC）是一种常见的恶性肿瘤，亟需开发药物和治疗靶点。铜死亡（cuproptosis）作为一种有前景的抑制肿瘤的机制而受到关注，因为铜稳态紊乱频繁发生于多种恶性肿瘤中。双硫仑（DSF）与铜离子联合使用（DSF/Cu）已被证明具有显著的抗肿瘤作用。本研究利用DSF/Cu探讨胃癌细胞中铜死亡的机制。用DSF/Cu处理胃癌细胞，并进行蛋白质测序以筛选差异表达基因。确定了过表达的 调控铜死亡及 表达的机制。随后，在胃癌小鼠模型中研究了如何提高DSF/Cu治疗胃癌的疗效。DSF/Cu在促进胃癌细胞铜死亡方面具有良好的治疗效果。蛋白质测序揭示 为 的下游基因。增加 的表达增强了胃癌细胞对铜处理的敏感性，并抑制了 的表达，从而发挥抗肿瘤作用。此外，将DSF/Cu负载于自然杀伤（NK）细胞来源的外泌体中，以增强DSF/Cu的生物安全性和肿瘤靶向性，并在体内和体外验证了对胃癌的抑制作用。本研究表明，DSF/Cu促进铜死亡，且 的表达影响胃癌的铜死亡敏感性。此外，NK细胞外泌体与DSF/Cu的联合提高了DSF/Cu的治疗效果，有助于促进胃癌的靶向治疗并提高临床适用性。
[英文摘要] Gastric cancer (GC) is a prevalent malignant tumor that warrants the development of drugs and therapeutic targets. Cuproptosis has emerged as a promising mechanism by which to inhibit tumors because copper homeostasis disorders frequently occur in various malignancies. The combination of disulfiram (DSF) and copper ions (DSF/Cu) has been shown to have significant antitumor effects. This study utilized DSF/Cu to investigate the mechanism underlying cuproptosis in GC cells. GC cells were treated with DSF/Cu and protein sequencing was performed to screen for differentially expressed genes. The mechanism by which overexpressed regulates cuproptosis and expression was determined. Subsequently, how to improve the efficacy of DSF/Cu in the treatment of GC was studied in a mouse model of GC. DSF/Cu had a good therapeutic effect on promoting cuproptosis in GC cells. Protein sequencing revealed as a downstream gene of . Increasing the expression of enhanced the sensitivity of GC cells to copper treatment and inhibited the expression of , thereby exerting an antitumor effect. Furthermore, DSF/Cu was loaded into exosomes derived from natural killer (NK) cells to enhance the biological safety and tumor targeting of DSF/Cu and validate the inhibitory effect on GC both and . This study showed that DSF/Cu promoted cuproptosis and the expression of affected cuproptosis sensitivity of GC. Moreover, the combination of NK cell exosomes with DSF/Cu improved the therapeutic effect of DSF/Cu, which helps to promote the targeted therapy of GC and improve clinical applicability.
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10. Myeloid cell reprogramming combined with zoledronic acid effectively suppresses bone metastasis.
PMID:日期:2026-07-27Bone metastases are refractory to current therapies, primarily owing to the immunosuppressive metastasis tumor microenvironment (TME), which is dominated by myeloid cells. However, the function and regulatory mechanisms of myeloid compartments within the bone TME are incompletely understood. Herein we sought to delineate the role of the DKK1-CKAP4 axis in shaping myeloid cell-mediated immunosuppression in bone metastases and to identify potential therapeutic strategies targeting this pathway. The composition and phenotypic characteristics of myeloid cells in the bone TME were analyzed. Mechanistic studies were conducted using co-culture systems and an (neutrophil-specific knockout) mouse model to delineate the role of the DKK1-CKAP4 axis in regulating neutrophil maturation, osteoclast-like cell differentiation, and macrophage polarization. The therapeutic efficacy of DKK1 blockade in combination with zoledronic acid, as well as the impact on remodeling the TME, was further validated in bone metastasis mouse models. Significant expansion and predominance of myeloid cells within the bone TME was noted. Mechanistically, the DKK1-CKAP4 axis regulated the development and function of multiple myeloid populations. The DKK1-CKAP4 axis drove neutrophils toward an immature-like, immunosuppressive phenotype, promoted osteoclast-like cell differentiation, and induced macrophage polarization into an M2-like phenotype. Importantly, combined therapy with DKK1 blockade and zoledronic acid reprogrammed immunosuppressive myeloid cells, restored antitumor immunity, and significantly reduced tumor burden in bone metastasis models. The findings herein showed the DKK1-CKAP4 axis to be a key regulator of myeloid-driven immunosuppression in the bone TME. The combination of DKK1 blockade with zoledronic acid represents a potential therapeutic strategy for bone metastases.