CANCER BIOLOGY & THERAPY癌症生物学与治疗
CANCER BIOLOGY & THERAPY(英文缩写 CANCER BIOL THER),ISSN 1538-4047,eISSN 1555-8576,中文译名:癌症生物学与治疗 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 | 4.875 | Q2 |
| 2022 | 3.600 | Q2 |
| 2023 | 4.400 | Q2 |
| 2024 | 4.600 | Q1 |
| 2025 | 5.700 | Q1 |
CANCER BIOLOGY & THERAPY 最新收录文献
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3. Statement of Retraction: STAT3-induced upregulation of long noncoding RNA HNF1A-AS1 promotes the progression of oral squamous cell carcinoma via activating Notch signaling pathway.
3. 撤稿声明：STAT3诱导的长链非编码RNA HNF1A-AS1上调通过激活Notch信号通路促进口腔鳞状细胞癌的进展PMID:日期:2026-09-29该文献暂无摘要。
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4. Statement of Retraction: Long non-coding RNA MEG3 suppresses the development of bladder urothelial carcinoma by regulating miR-96 and TPM1.
4. 撤稿声明：长链非编码RNA MEG3通过调控miR-96和TPM1抑制膀胱尿路上皮癌的发展PMID:日期:2026-09-29该文献暂无摘要。
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5. Elevated miR-103b in exosomes derived from brain-metastatic triple-negative breast cancer cells remodels the brain pre-metastatic niche (PMN).
5. 脑转移性三阴性乳腺癌细胞来源外泌体中升高的miR-103b重塑脑转移前生态位（PMN）PMID:日期:2026-09-25Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer with high brain metastatic (BM) potential. Tumor-derived exosomes are implicated as key modulators during the formation of the pre-metastatic niche (PMN). However, the regulation of TNBC-BM-derived exosomes on brain PMN remains enigmatic. The morphology and uptake of exosomes were identified using transmission electron microscopy and live-cell imaging, respectively. Differentially secreted miRNAs and mRNA were identified using high-throughput sequencing. The permeability of the blood‒brain barrier (BBB) and tight junction integrity were examined using immunofluorescence staining. Cell viability was examined using the CCK-8 assay. The apoptosis and intracellular ROS were investigated using fluorescence staining. The expression of mRNAs was examined using qPCR. miR-103b was significantly increased in exosomes derived from TNBC-BM cells. miR-103b compromised the tight junctions of HUVECs and increased BBB permeability in mice. Additionally, miR-103b promoted apoptosis and increased intracellular ROS in HUVECs and U251 cells, two cell lines commonly used as surrogates for brain microvascular endothelial cells and astrocytes, respectively. miR-103b-regulated differentially expressed genes modulated tight junction, apoptosis, oxidative stress, inflammation, and metabolism. Target analysis identified 216 targets of miR-103b, among which hub targets were associated with biological processes involved in maintaining the BBB and the glucose metabolism signaling pathway. Collectively, our findings for the first time reveal that exosomal miR-103b from TNBC-BM cells potentially regulates the two major cellular constituents of the brain PMN, highlighting its role in the formation of the brain PMN during TNBC-BM and its potential as a promising therapeutic target.
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6. Fibroblast-associated TPM2 links cell-matrix remodeling to EMT-Notch signaling and gemcitabine resistance in intrahepatic cholangiocarcinoma.
6. 成纤维细胞相关的TPM2将细胞基质重塑与肝内胆管癌中的EMT-Notch信号传导及吉西他滨耐药性联系起来PMID:日期:2026-09-21Intrahepatic cholangiocarcinoma (ICC) is an aggressive liver malignancy with heterogeneous responses to gemcitabine-based chemotherapy. The cellular and microenvironmental programs associated with the gemcitabine response remain incompletely understood. This study aimed to identify tumor microenvironment-associated regulators of gemcitabine response in ICC and evaluate their functional relevance using patient-derived organoids. Four public single-cell RNA sequencing datasets comprising 50,176 cells were integrated with TCGA-based transcriptomic and drug sensitivity analyses. High-dimensional weighted gene co-expression network analysis was used to identify cell type-associated modules. Predicted gemcitabine IC50-related differentially expressed genes were intersected with the fibroblast-associated module genes. Patient-derived ICC organoids were used for gemcitabine sensitivity testing and CRISPR/Cas9-mediated TPM2 knockout validation. Single-cell analysis revealed fibroblast enrichment in ICC, and co-expression analysis identified fibroblast-associated modules enriched in extracellular matrix organization and ECM-receptor interaction. Integrated analysis identified TPM2 as a fibroblast-enriched candidate associated with poor prognosis, activation of epithelial-mesenchymal transition, TGF- and Notch-related pathways, and dynamic cellular state transitions. Patient-derived ICC organoids retained features of matched tumors and showed distinct gemcitabine sensitivities that were broadly consistent with the clinical imaging responses. In a relatively gemcitabine-resistant organoid model, TPM2 knockout enhanced gemcitabine-induced cytotoxicity and suppressed EMT/ECM-related programs and Notch signaling. These findings identify TPM2-associated cell-matrix remodeling as a potential contributor to gemcitabine resistance in ICC and support patient-derived organoids as a functional platform for studying therapeutic vulnerabilities.
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7. DNA-PKcs and PARP1 at the interface between DNA damage responses and cGAS-STING signaling: context-dependent roles and therapeutic implications.
7. DNA-PKcs和PARP1在DNA损伤反应与cGAS-STING信号传导交界处的作用：情境依赖性角色及治疗意义PMID:日期:2026-09-08To explore the roles of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and poly(ADP-ribose) polymerase 1 (PARP1) in both the DNA damage repair (DDR) pathway and the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway mediated immune response, and to analyze the therapeutic potential of their inhibitors. This is a review article synthesizing recent findings on the functions of DNA-PKcs and PARP1 in DDR, their context-dependent effects on the cGAS-STING pathway and the therapeutic mechanisms of their inhibitors. DNA-PKcs and PARP1 are key components of two major DDR mechanisms. Beyond their canonical repair functions, both factors significantly regulate the cGAS-STING pathway, a central mediator linking cytoplasmic DNA and the type I interferon response. DNA-PKcs and PARP1 connect genome maintenance with innate immune signaling through context-dependent mechanisms. Targeting these proteins represents a promising strategy for modulating cGAS-STING signaling and improving disease treatment.
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8. Thioredoxin reductase-1 facilitates cellular plasticity and stemness mediated by TGF-β1 in non-small cell lung cancer.
8. 硫氧还蛋白还原酶-1促进非小细胞肺癌中TGF-β1介导的细胞可塑性和干性PMID:日期:2026-09-08Cellular plasticity and epithelial-mesenchymal transition (EMT) promote the initiation and progression of non-small cell lung cancer (NSCLC). Thioredoxin reductase 1 (TXNRD1), a key redox enzyme, has been linked to malignancy, but its mechanism in NSCLC remains unclear. We examined whether TXNRD1 regulates TGF-β1 autocrine signaling to drive EMT and stemness. Stage-progression gene profiles were analyzed in the TCGA and GEO databases with an emphasis on redox gene families. TXNRD1 was manipulated by overexpression or knockdown in A549, H226, and H1299 cells, followed by migration/invasion, spheroid assays, ELISA for cytokines, and RT-qPCR/Western blot for EMT markers. RNA-seq with pathway enrichment analyses was used to identify downstream programs. An orthotopic lung cancer mouse model was established using TXNRD1-WT cells, TXNRD1-deficient cells, and TXNRD1-deficient cells treated with TRi-1. Tumor progression was monitored by bioluminescence imaging at 6 and 12 weeks after transplantation. TXNRD1 expression was ~2-fold higher in advanced-stage NSCLC and was validated in tumor tissues. CRISPR/Cas9 or siRNA knockdown reduced EMT-associated genes and decreased TGF-β1 production in A549 and H226 cells. TXNRD1 overexpression increased EMT and stemness markers and produced larger, more compact spheres with higher sphere numbers in H1299 cells. RNA-seq indicated the TXNRD1 pathway activates the TGF-β1 pathway to promote EMT, motility, and stemness via an autocrine loop; knockdown or TXNRD1 inhibition suppressed metastatic tumor growth in vivo. Our study identifies TXNRD1 as a crucial regulator of cellular plasticity and metastasis in NSCLC via the TGF-β1 pathway, suggesting that targeting TXNRD1 may reduce metastatic potential and improve patient survival.
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9. Synchronizing immunity and angiogenesis in lung adenocarcinoma: bridging biological synergy and clinical translation.
PMID:日期:2026-09-08The recent study by Liu et al. provided compelling preclinical evidence that lenvatinib enhances the efficacy of combined radiotherapy and PD-L1 blockade by modulating both angiogenesis and antitumor immunity in lung adenocarcinoma. In this correspondence, I discuss the translational implications of these findings and highlight several challenges that should be addressed before clinical implementation. These include the molecular heterogeneity of lung adenocarcinoma, interpatient variability in the temporal dynamics of vascular normalization and immune activation, and the limitations of relying solely on PD-L1 expression for patient selection. I further emphasize the need for biomarker-driven and adaptive clinical trial designs incorporating functional imaging, circulating biomarkers, and immune monitoring to optimize treatment timing and identify patients most likely to benefit from this therapeutic strategy. These considerations may facilitate the successful translation of promising preclinical observations into precision radioimmunotherapy for lung adenocarcinoma.
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10. The molecular mechanisms of platelets in tumor invasion and metastasis: a controversial role.
10. 血小板在肿瘤侵袭和转移中的分子机制：一个有争议的作用PMID:日期:2026-08-11[中文摘要] 血小板传统上被认为在止血中发挥作用，如今人们认识到其还积极参与肿瘤进展、血管生成和转移。通过与癌细胞的动态双向相互作用，血小板在计数、平均血小板体积以及分子货物（包括蛋白质和mRNA）方面发生可测量的改变，支持其作为液体活检生物标志物用于早期癌症检测的潜在用途。在肿瘤微环境中，血小板有助于免疫逃逸，支持肿瘤细胞的内渗和外渗，增强循环肿瘤细胞的存活，并促进新生血管形成。此外，它们还能物理性地屏蔽恶性细胞免受免疫监视，从而增加转移潜能。尽管已有背景特异性的抗肿瘤效应报道，但主要证据支持血小板在很大程度上具有促肿瘤和促转移作用。因此，阐明血小板-肿瘤相互作用的分子机制对于改善癌症风险分层、预后评估和治疗开发至关重要。本综述总结了血小板衍生生物标志物的当前进展，并讨论了靶向血小板介导通路以抑制转移和改善癌症患者临床结局的新兴治疗策略。
[英文摘要] Platelets, traditionally recognized for their role in hemostasis, are now understood to actively contribute to tumor progression, angiogenesis, and metastasis. Through dynamic bidirectional interactions with cancer cells, platelets undergo measurable alterations in count, mean platelet volume, and molecular cargo, including proteins and mRNAs, supporting their potential utility as liquid biopsy biomarkers for early cancer detection. Within the tumor microenvironment, platelets contribute to immune evasion, support tumor cell intravasation and extravasation, enhance the survival of circulating tumor cells, and promote neovascularization. In addition, they can physically shield malignant cells from immune surveillance, thereby increasing metastatic potential. Although context-specific anti-tumor effects have been reported, the predominant evidence supports a largely pro-tumorigenic and pro-metastatic role for platelets. Elucidating the molecular mechanisms underlying platelet-tumor interactions is therefore essential for improving cancer risk stratification, prognostic evaluation, and therapeutic development. This review summarizes current advances in platelet-derived biomarkers and discusses emerging therapeutic strategies targeting platelet-mediated pathways to suppress metastasis and improve clinical outcomes in cancer patients.