Seminars in cancer biology最新文献

英文中文

Spatial multi-omics in precision medicine: Integrating biological insights through multidisciplinary collaboration 精准医学中的空间多组学：通过多学科合作整合生物学见解。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-12-29 DOI: 10.1016/j.semcancer.2025.12.009

Da Yeon Kim , Jeeyong Lee , Jiwon Choi , Hayeon Shin , Jason S. Lee , Eun Ju Kim

Spatial multi-omics has emerged as a transformative approach in biomedical research, enabling the integration of diverse molecular modalities while preserving their native spatial contexts. This review provides an overview of spatial multi-omics technologies, focusing on data acquisition, quality management, and integration strategies across transcriptomic, genomic, epigenomic, proteomic, and metabolomic layers. Spatial transcriptomics is highlighted as a foundational framework for aligning multi-omics data with histological and cellular architecture. We emphasize its applications in elucidating tumor heterogeneity, immune–stromal interactions, and metabolic or epigenetic dynamics within the tumor microenvironment, which are crucial for understanding disease progression and therapeutic response. The review further discusses key challenges such as technical noise, batch effects, and the complexity of high-dimensional data integration, along with optimization strategies for sampling and analysis in both clinical and research settings. Ethical and regulatory considerations, including patient data privacy and responsible implementation of artificial intelligence, are also examined in the context of clinical translation. Taken together, this review offers an integrative synthesis of spatial multi-omics technologies and their applications in cancer biology, providing a balanced perspective to help researchers and clinicians navigate this rapidly evolving field and recognize its translational potential for advancing precision medicine.

空间多组学已成为生物医学研究中的一种变革性方法，使各种分子形态能够整合，同时保留其原有的空间背景。本文综述了空间多组学技术，重点介绍了转录组学、基因组学、表观基因组学、蛋白质组学和代谢组学层面的数据采集、质量管理和整合策略。空间转录组学被强调为与组织和细胞结构对齐多组学数据的基础框架。我们强调其在阐明肿瘤异质性、免疫-基质相互作用以及肿瘤微环境中的代谢或表观遗传动力学方面的应用，这对于理解疾病进展和治疗反应至关重要。该综述进一步讨论了关键挑战，如技术噪声、批处理效应和高维数据集成的复杂性，以及临床和研究环境中采样和分析的优化策略。伦理和监管方面的考虑，包括患者数据隐私和人工智能的负责任实施，也在临床翻译的背景下进行了检查。综上所述，本文综述了空间多组学技术及其在癌症生物学中的应用，为研究人员和临床医生导航这一快速发展的领域提供了一个平衡的视角，并认识到其在推进精准医学方面的转化潜力。

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引用次数: 0

Targeting aging-related signaling pathways for cancer therapy 靶向衰老相关信号通路的癌症治疗。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-12-23 DOI: 10.1016/j.semcancer.2025.12.007

Hiroyuki Inuzuka, Wenyi Wei

引用次数: 0

Heartbreakers and healers: RNA rebels in cardio-oncology 心碎者和治愈者：心脏肿瘤学中的RNA叛军。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-12-23 DOI: 10.1016/j.semcancer.2025.12.008

Celestina Agyemang-Dua , Charles S. Chung , Cristina Espinosa-Diez

Cancer therapies save lives but often “break hearts” by damaging the cardiovascular system. As survival improves, therapy-induced cardiotoxicity has become a defining challenge of modern oncology. Recent discoveries reveal that long non-coding RNAs (lncRNAs), once dismissed as genomic noise, are the “RNA rebels” orchestrating cellular responses to cancer treatments. These molecules act as both heartbreakers and healers, amplifying or counteracting oxidative stress, mitochondrial dysfunction, apoptosis, and vascular injury. In anthracycline, radiation, and VEGF-targeted therapies, lncRNAs govern key processes that dictate whether cells succumb to damage or mount protective repair responses. Pro-injury lncRNAs exacerbate senescence and inflammation, while protective ones preserve mitochondrial homeostasis and limit cell death. Beyond mechanistic insight, these molecules hold clinical promise as biomarkers and therapeutic targets, guiding RNA-based strategies to predict, prevent, and treat cardiotoxicity. Understanding how they blur the line between protection and harm may redefine how we safeguard the heart in the era of precision cardio oncology.

癌症治疗可以挽救生命，但往往会因损害心血管系统而“伤透了心”。随着生存率的提高，治疗性心脏毒性已成为现代肿瘤学的一个决定性挑战。最近的发现表明，长链非编码RNA (lncRNAs)，曾经被认为是基因组噪音，是“RNA反叛者”，协调细胞对癌症治疗的反应。这些分子既能让人心碎，也能治愈，它们能放大或抵消氧化应激、线粒体功能障碍、细胞凋亡和血管损伤。在蒽环类药物、放疗和vegf靶向治疗中，lncrna控制着决定细胞是否屈服于损伤或产生保护性修复反应的关键过程。亲损伤lncrna会加剧衰老和炎症，而保护性lncrna会维持线粒体稳态并限制细胞死亡。除了机理之外，这些分子作为生物标志物和治疗靶点具有临床前景，指导基于rna的策略来预测、预防和治疗心脏毒性。了解它们是如何模糊保护和伤害之间的界限的，可能会重新定义我们在精确心脏肿瘤学时代如何保护心脏。

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引用次数: 0

Immune checkpoint inhibitor-induced myocarditis: focus on the downstream pathogenic components and potential therapeutics 免疫检查点抑制剂诱导的心肌炎：关注下游致病成分和潜在治疗方法。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-12-18 DOI: 10.1016/j.semcancer.2025.12.004

Yifan Chen , Xuejun Wang , Yihui Shen , Hui Zhang , Cheng Yu , Leilei Cheng , Junbo Ge

Advent of immune checkpoint inhibitors (ICIs) has renovated onco-immunotherapy, with around 50 % of cancer patients suitable for the treatment. However, patients treated by ICIs are in jeopardy for immune-related adverse events (irAEs) that attack any organ including the heart. ICIs-induced myocarditis (ICIIM) is an uncommon but possibly fatal irAE. With the increasing use of ICIs and improved diagnosis of this disease, the incidence of ICIIM is growing rapidly. In this review, we briefly overview roles of T cells and their immune checkpoints, and categorize the pathogenic process of ICIIM into three stages (upstream, midstream and downstream), with addressing recent research progress on the pathogenic mechanisms in each stage, particularly focusing on the downstream core pathogenic components and potential therapeutics for this disease.

免疫检查点抑制剂（ICIs）的出现革新了肿瘤免疫治疗，约50%的癌症患者适合这种治疗。然而，接受ICIs治疗的患者处于免疫相关不良事件（irAEs）的危险之中，这些不良事件会攻击包括心脏在内的任何器官。icis诱导的心肌炎（ICIIM）是一种罕见但可能致命的心肌炎。随着ici使用的增加和该病诊断的改善，icim的发病率正在迅速增长。本文将简要概述T细胞及其免疫检查点的作用，并将ICIIM的发病过程分为上游、中游和下游三个阶段，介绍了各阶段发病机制的最新研究进展，重点介绍了该疾病下游的核心致病成分和潜在的治疗方法。

引用次数: 0

Obesity and GEP-NEN: what’s new? 肥胖和GEP-NEN：有什么新进展？

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-12-15 DOI: 10.1016/j.semcancer.2025.12.006

M. Boschetti , I. Hasballa , I. Patelli , G. Piras , M. Albertelli

Gastroenteropancreatic neuroendocrine neoplasms (GEP-NEN) comprise a heterogeneous group of tumors differing according to the primary lesion site, histological features, clinical status and prognosis. The etiopathogenesis of GEP-NEN is not fully elucidated, however, excessive visceral adiposity may play a role in NEN oncogenesis and pose challenges to NEN therapeutic management. The interplay between obesity and GEP-NEN is complex and the potential carcinogenic mechanisms of obesity include chronic inflammation, abnormal immune function, hormone and metabolic dysregulation. Data regarding the prognostic impact of visceral adiposity on patients’ clinical and survival outcomes is still very limited and indeterminate. Molecular evidence predominantly supports the carcinogenic effects of obesity, although some studies have documented a potential protective role of excessive adiposity, i.e. the “obesity paradox” phenomenon, in NENs. Concerning therapeutic management of obesity in the setting of GEP-NENs, the current strategies to be considered include first-line nutritional and lifestyle intervention, followed by pharmacological and surgical treatment. This review aims to explore the intricate relationship between obesity and GEP-NENs, the potential impact on NEN outcomes, the current treatment approaches and future perspectives of the therapeutic landscape of individuals affected by GEP-NEN and obesity.

胃肠胰神经内分泌肿瘤（GEP-NEN）是一种异质性肿瘤，根据原发病变部位、组织学特征、临床状态和预后而有所不同。GEP-NEN的发病机制尚不完全清楚，然而，过度的内脏脂肪可能在NEN的肿瘤发生中起作用，并对NEN的治疗管理提出了挑战。肥胖与GEP-NEN之间的相互作用是复杂的，肥胖的潜在致癌机制包括慢性炎症、免疫功能异常、激素和代谢失调。关于内脏脂肪对患者临床和生存结果的预后影响的数据仍然非常有限和不确定。分子证据主要支持肥胖的致癌作用，尽管一些研究已经记录了过度肥胖的潜在保护作用，即NENs中的“肥胖悖论”现象。关于GEP-NENs背景下肥胖的治疗管理，目前需要考虑的策略包括一线营养和生活方式干预，其次是药物和手术治疗。本文旨在探讨肥胖与GEP-NEN之间的复杂关系，对NEN结果的潜在影响，目前的治疗方法和未来治疗前景对GEP-NEN和肥胖个体的影响。

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引用次数: 0

Protein lactylation in cancer and other pathologies: Epigenetic regulation of glycolysis and its therapeutic perspectives 癌症和其他病理中的蛋白质乳酸化：糖酵解的表观遗传调控及其治疗前景。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-12-11 DOI: 10.1016/j.semcancer.2025.12.005

Yaowen Zhang , Jianxiang Wang , Cong Li , Zhe Lei , Xiang Zhao , Xuan Xuan , Olga Sukocheva , Edmund Tse , Junqi Liu

Lactylation, a recently recognized post-translational protein modification, is reshaping research in epigenetics and molecular medicine. Emerging evidence indicates that lactylation plays a critical role in the onset and progression of cancer, as well as in several pre-cancerous and metabolism-associated pathologies. This review summarizes the current understanding of the mechanisms and biological roles of lactylation in cancer and other diseases. Lactate has been shown to promote carcinogenesis both as an additional energy source and as a signaling molecule. Glycolysis and glucose transport—major sources of lactate and subsequent lactylation—are frequently targeted by anti-cancer therapies. Several small-molecule glucose transporter type 1 (GLUT1) inhibitors, including STF-31, WZB-117, and BAY-876, have demonstrated efficacy in suppressing tumor growth. During lactylation, lactate is covalently attached to histone lysine residues, leading to epigenetic modifications. This process is regulated by “writer” enzymes (p300 and HBO1) and “eraser” enzymes (HDAC1–3 and SIRT1–3), which participate in nuclear signaling networks associated with oncogenic transformation. Several inhibitors targeting “writer” enzymes, such as A485 and andrographolide, have been developed and shown to suppress angiogenesis. Inhibition of tumor immune evasion has also been explored using glycolytic enzyme inhibitors, including 2-deoxy-D-glucose and oxalate. Despite these advances, lactylation-targeted research remains in its early stages and faces notable limitations that warrant further investigation. This review provides insights into the role of lactylation in diverse diseases and highlights emerging therapeutic strategies aimed at modulating lactylation-associated molecular targets.

乳酸酰化是一种最近被认可的翻译后蛋白质修饰，正在重塑表观遗传学和分子医学的研究。新出现的证据表明，乳酸酰化在癌症的发生和进展以及一些癌前病变和代谢相关病变中起着关键作用。本文综述了目前对乳酸化在癌症和其他疾病中的机制和生物学作用的认识。乳酸作为一种额外的能量来源和一种信号分子已被证明可以促进癌变。糖酵解和葡萄糖转运-乳酸的主要来源和随后的乳酸化-经常是抗癌治疗的目标。几种小分子葡萄糖转运蛋白1型（GLUT1）抑制剂，包括STF-31、WZB-117和BAY-876，已被证明具有抑制肿瘤生长的功效。在乳酸化过程中，乳酸共价附着在组蛋白赖氨酸残基上，导致表观遗传修饰。这一过程受“书写者”酶（p300和HBO1）和“擦除者”酶（HDAC1-3和SIRT1-3）调控，它们参与与致癌转化相关的核信号网络。一些靶向“writer”酶的抑制剂，如A485和穿心花内酯，已经被开发出来并被证明可以抑制血管生成。利用糖酵解酶抑制剂，包括2-脱氧-d -葡萄糖和草酸盐，也对肿瘤免疫逃避的抑制进行了探索。尽管取得了这些进展，针对乳酸酰化的研究仍处于早期阶段，面临着值得进一步研究的显著局限性。本文综述了乳酸化在多种疾病中的作用，并强调了旨在调节乳酸化相关分子靶点的新兴治疗策略。

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引用次数: 0

Leveraging cancer metabolism to translate into effective therapeutics 利用癌症代谢转化为有效的治疗方法。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-12-11 DOI: 10.1016/j.semcancer.2025.12.003

Jie Xu , Linlin Guo , Yi Wang , Xiaoping Li , Ping Yi , Chunming Cheng

Abnormal metabolism is a typical characteristic of malignant tumors, broadly influencing the outcome of cancer therapy. Research on tumor metabolism has increased exponentially in last decades. There is an urgent need to provide a blueprint or framework to accelerate the translation of cancer metabolism research into effective therapeutics. In this review, we summarize the impact of metabolism on cancer progression and emerging metabolic therapies, and systematically outline potential clinical applications in cancer prevention, early screening, diagnosis, treatment, and new challenges. Furthermore, we aim to provide researchers and clinicians with a clearer perspective on the immediate translation of clinical applications stemming from cancer metabolism research. It will revolutionize cancer management and significantly enhance patient survival.

代谢异常是恶性肿瘤的典型特征，广泛影响肿瘤治疗的结果。近几十年来，对肿瘤代谢的研究呈指数级增长。迫切需要提供一个蓝图或框架来加速将癌症代谢研究转化为有效的治疗方法。在这篇综述中，我们总结了代谢对癌症进展的影响和新兴的代谢疗法，并系统地概述了在癌症预防、早期筛查、诊断、治疗和新挑战方面的潜在临床应用。此外，我们的目标是为研究人员和临床医生提供一个更清晰的视角，了解来自癌症代谢研究的临床应用的即时翻译。它将彻底改变癌症管理，显著提高患者生存率。

引用次数: 0

Microbiota and cancer immunotherapy: Mechanisms, clinical implications, and precision therapeutics 微生物群和癌症免疫治疗：机制、临床意义和精确治疗。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-12-05 DOI: 10.1016/j.semcancer.2025.12.002

Dongliang Wei , Yilan Sun , Jing Han , Jiannan Liu

The microbiota has emerged as a pivotal modulator of cancer immunotherapy, offering novel insights into the efficacy and toxicity of immune checkpoint inhibitors (ICIs). Recent evidence highlights that microbial communities and their metabolites dynamically regulate host immunity by priming dendritic cells, enhancing T-cell infiltration, and reprogramming the tumor microenvironment. Microbiome dysbiosis is implicated in immune-related adverse events (irAEs), underscoring its dual role in therapeutic outcomes. Leveraging these findings, precision microbiome interventions, including fecal microbiota transplantation, engineered probiotics, and dietary modulation, which demonstrate potential to enhance ICIs responsiveness and mitigate irAEs in preclinical and early-phase clinical studies. However, translating these strategies into clinical practice requires rigorous validation through multicenter trials to establish safety, efficacy, and standardized protocols. This review synthesizes current knowledge on the microbiome-immune-oncology axis, with a focus on mechanistic underpinnings, translational challenges, and innovative therapeutic strategies. By integrating microbiome profiling with patient-specific factors, proposing a roadmap for personalized immunotherapy, aligning with the emerging paradigm of precision oncology.

微生物组已成为癌症免疫治疗的关键调节剂，为免疫检查点抑制剂（ICIs）的疗效和毒性提供了新的见解。最近的证据表明，微生物群落及其代谢物通过启动树突状细胞、增强t细胞浸润和重新编程肿瘤微环境来动态调节宿主免疫。微生物群失调与免疫相关不良事件（irAEs）有关，强调其在治疗结果中的双重作用。利用这些发现，精确的微生物组干预，包括粪便微生物群移植、工程益生菌和饮食调节，在临床前和早期临床研究中显示出增强ICIs反应性和减轻irae的潜力。然而，将这些策略转化为临床实践需要通过多中心试验进行严格的验证，以建立安全性、有效性和标准化方案。这篇综述综合了微生物组-免疫-肿瘤学轴的当前知识，重点是机制基础，转化挑战和创新治疗策略。通过将微生物组分析与患者特异性因素相结合，提出个性化免疫治疗的路线图，与新兴的精准肿瘤学范式保持一致。

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引用次数: 0

Integrating biomarkers, experimental models, genomics, and novel therapeutics for pancreatic cancer precision medicine 整合生物标志物、实验模型、基因组学和胰腺癌精准医学的新疗法

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-12-04 DOI: 10.1016/j.semcancer.2025.12.001

Luca Morelli

引用次数: 0

Expression of concern "Decoding T cell senescence in cancer: Is revisiting required?" [Semin. Cancer Biol. 108 (2025) 33-47]. “解码癌症中的T细胞衰老：是否需要重访？”[Semin。中国生物医学工程学报，2014,33(5):447 - 447。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-12-01 Epub Date: 2025-11-08 DOI: 10.1016/j.semcancer.2025.11.018

引用次数: 0

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