Seminars in cancer biology最新文献_第9页

Obesity-driven inflammation and cancer risk: A comprehensive review 肥胖引发的炎症和癌症风险：一项全面的综述。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-07-25 DOI: 10.1016/j.semcancer.2025.07.007

D.A. Lamabadusuriya , H. Jayasena , A.K. Bopitiya , A.D. De Silva , P. Jayasekera

Obesity is a growing global health challenge, significantly increasing the risk of metabolic diseases and cancer. This review explores the link between obesity-driven inflammation and cancer risk, emphasizing the key biological mechanisms. Chronic low-grade inflammation in obesity, mediated by dysfunctional adipose tissue, promotes a pro-tumorigenic microenvironment through increased secretion of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β. These factors contribute to insulin resistance, oxidative stress, and immune cell infiltration, fostering tumorigenesis. Adipokine imbalances, particularly elevated leptin and reduced adiponectin levels, further drive cancer progression by enhancing cell proliferation, angiogenesis, and immune evasion. Additionally, obesity-induced hypoxia, endoplasmic reticulum stress, and gut microbiome dysbiosis amplify systemic inflammation and metabolic dysfunction, further increasing cancer susceptibility. Epidemiological evidence highlights strong associations between obesity and cancers such as breast, colorectal, liver, and pancreatic cancer. Given the rising global prevalence of obesity, addressing inflammation-mediated oncogenesis is crucial. Lifestyle modifications, including weight loss through dietary and physical activity interventions, have demonstrated significant cancer risk reduction. Emerging pharmacological approaches targeting inflammatory pathways and adipokine regulation offer promising therapeutic potential. Understanding the mechanisms linking obesity, inflammation, and cancer provides valuable insights for developing targeted prevention and treatment strategies.

肥胖是一个日益严重的全球健康挑战，显著增加了患代谢性疾病和癌症的风险。这篇综述探讨了肥胖驱动的炎症与癌症风险之间的联系，强调了关键的生物学机制。肥胖的慢性低度炎症，由功能失调的脂肪组织介导，通过增加促炎细胞因子如TNF-α、IL-6和IL-1β的分泌，促进促肿瘤微环境。这些因素有助于胰岛素抵抗、氧化应激和免疫细胞浸润，促进肿瘤发生。脂肪因子失衡，特别是瘦素升高和脂联素水平降低，通过促进细胞增殖、血管生成和免疫逃逸，进一步推动癌症进展。此外，肥胖引起的缺氧、内质网应激和肠道微生物群失调会放大全身炎症和代谢功能障碍，进一步增加癌症易感性。流行病学证据强调肥胖与乳腺癌、结直肠癌、肝癌和胰腺癌等癌症之间存在密切联系。鉴于全球肥胖患病率的上升，解决炎症介导的肿瘤发生至关重要。生活方式的改变，包括通过饮食和身体活动干预来减轻体重，已经证明可以显著降低癌症风险。针对炎症途径和脂肪因子调节的新兴药理学方法提供了有希望的治疗潜力。了解肥胖、炎症和癌症之间的联系机制，为制定有针对性的预防和治疗策略提供了有价值的见解。

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引用次数: 0

Host-microbiota interactions in genitourinary cancer immunotherapy 泌尿生殖系统癌免疫治疗中的宿主-微生物相互作用。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-07-23 DOI: 10.1016/j.semcancer.2025.07.005

Xiao-Feng Xu , Jin-Long Cui , Wen-Hua Li , Yi-Hang Xu , Shuai Yuan , Xian-Tao Zeng , Bing-Hui Li

Immunotherapy for genitourinary cancer, including bladder cancer, renal cell carcinoma, and prostate cancer, has made significant progress in recent years; however, it still faces challenges such as low patient response rates, drug resistance and immune-related adverse events. As the “second genome” of the human body, the gut microbiota plays a key factor in modulating the host immune response. Studies have shown that host-microbiome interactions profoundly affect the efficacy and safety of immune checkpoint inhibitors by shaping the tumor immune microenvironment (TIME). This review systematically analyzes the mechanisms by which urinary system-specific microbiota (such as urothelial bacteria and gut microbiota) regulate TIME through metabolic regulation, immune cell function remodeling, and inflammatory signaling networks. We further explore the clinical translational strategy targeting the microbiome to enhance immunotherapy responses, providing new perspectives for precision immunotherapy of urinary tumors.

免疫治疗泌尿生殖系统癌，包括膀胱癌、肾细胞癌和前列腺癌，近年来取得了重大进展；然而，它仍然面临着诸如患者反应率低、耐药和免疫相关不良事件等挑战。肠道菌群作为人体的“第二基因组”，在调节宿主免疫反应中起着关键作用。研究表明，宿主-微生物组相互作用通过塑造肿瘤免疫微环境（TIME）深刻影响免疫检查点抑制剂的疗效和安全性。本文系统分析了泌尿系统特异性微生物群（如尿路上皮细菌和肠道微生物群）通过代谢调节、免疫细胞功能重塑和炎症信号网络调节TIME的机制。我们进一步探索以微生物组为靶点增强免疫治疗应答的临床转化策略，为泌尿系肿瘤的精准免疫治疗提供新的视角。

引用次数: 0

Landscape of non-coding RNAs in cancer treatment-induced cardiovascular toxicity: From mechanistic insights to clinical implications 非编码rna在癌症治疗诱导的心血管毒性中的作用：从机制到临床意义。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-07-21 DOI: 10.1016/j.semcancer.2025.07.009

Yayu Chen , Zhishuang Ye , Rong-Quan He , Gang Chen , Daniel Xin Zhang

Non-coding RNAs (ncRNAs) are increasingly recognized as crucial regulators in the pathophysiology of cancer treatment–induced cardiovascular toxicity, which largely stems from their capacity to orchestrate a wide range of gene expression networks. Emerging evidence has uncovered complex and critical functions of ncRNAs, including microRNAs, long non-coding RNAs, and circular RNAs, in mediating cardiotoxicity during cancer treatment. Here, we revisit the mechanisms of major anti-cancer treatment modalities and detail how they may lead to cardiovascular toxicity, which involves a myriad of key, interconnected processes, such as apoptosis, DNA damage, oxidative stress, mitochondrial damage, and autophagy. We further underscore the pivotal roles of ncRNAs within the cardio-oncology landscape mechanistically and analyze their clinical potentials to predict, detect, and treat cardiovascular damage in oncology settings. With this review, we aim to provide a comprehensive and up-to-date landscape of ncRNAs in the rapidly revolving field of cancer treatment–related cardiovascular toxicity, highlighting how such fundamental discoveries may guide future clinical applications.

非编码rna （ncRNAs）越来越被认为是癌症治疗诱导的心血管毒性病理生理学中的关键调节因子，这主要源于它们协调广泛的基因表达网络的能力。新出现的证据揭示了ncRNAs（包括microRNAs、长链非编码rna和环状rna）在癌症治疗过程中介导心脏毒性的复杂和关键功能。在这里，我们回顾了主要抗癌治疗方式的机制，并详细介绍了它们如何导致心血管毒性，这涉及无数关键的，相互关联的过程，如细胞凋亡，DNA损伤，氧化应激，线粒体损伤和自噬。我们进一步强调了ncrna在心脏肿瘤学领域的关键作用，并分析了它们在肿瘤环境中预测、检测和治疗心血管损伤的临床潜力。通过这篇综述，我们的目标是在快速发展的癌症治疗相关心血管毒性领域提供一个全面和最新的ncrna景观，强调这些基础发现如何指导未来的临床应用。

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引用次数: 0

Cancer prevention and interception with antidiabetic and anti-obesity drugs: Current and future perspectives 用抗糖尿病和抗肥胖药物预防和阻断癌症：当前和未来的观点。

IF 15.7 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-07-21 DOI: 10.1016/j.semcancer.2025.07.008

Adriana Albini , Anna Rita Cantelmo , Lorenzo Mortara , Douglas M. Noonan , Giovanni Corso

Obesity and type 2 diabetes are major risk factors for cardiovascular diseases and multiple malignancies, and epidemiology reveals an increasing burden of obesity-related cancers, in particular liver, pancreatic and endometrial. Obesity is also clearly associated with an increased risk of breast cancer, particularly in postmenopausal women. Chronic hyperinsulinemia, systemic inflammation, and metabolic dysregulation create a tumor-promoting environment, emphasizing the need for interventions that target metabolic health and can provide cancer prevention or interception. This review examines the potential cancer-preventive effects of antidiabetic and anti-obesity drugs, summarizing current preclinical and clinical evidence on their mechanisms and efficacy. Among these agents, metformin has been extensively studied, demonstrating anticancer properties through AMP-activated protein kinase activation, mammalian target of rapamycin inhibition, and reduced insulin-like growth factor 1 signaling. Glucagon-like peptide-1 receptor agonists, including semaglutide and tirzepatide, promote weight loss, insulin sensitivity, and anti-inflammatory effects, with emerging evidence suggesting direct tumor-suppressive actions. Sodium-glucose cotransporter 2 inhibitors modulate tumor metabolism by reducing glucose availability and mitigating systemic inflammation. Other agents, including dipeptidyl peptidase-4 inhibitors, thiazolidinediones, sulfonylureas, and alpha-glucosidase inhibitors, have shown mixed evidence regarding their potential anticancer effects, necessitating further investigation. While observational studies and meta-analyses suggest a potential reduction in cancer risk with certain antidiabetic and anti-obesity agents, randomized controlled trials specifically assessing cancer prevention are limited. Additionally, long-term safety concerns, including potential tumor-promoting effects in specific contexts, warrant further investigation. Future research should focus on large-scale clinical trials and mechanistic studies to validate the oncologic benefits and risks of these agents.

肥胖和2型糖尿病是心血管疾病和多种恶性肿瘤的主要危险因素，流行病学显示，肥胖相关癌症的负担日益增加，特别是肝脏、胰腺和子宫内膜癌。肥胖也明显与乳腺癌风险增加有关，尤其是绝经后妇女。慢性高胰岛素血症、全身性炎症和代谢失调创造了促进肿瘤的环境，强调了针对代谢健康的干预措施的必要性，并可以提供癌症预防或阻断。本文综述了抗糖尿病和抗肥胖药物的潜在癌症预防作用，总结了目前关于其机制和疗效的临床前和临床证据。在这些药物中，二甲双胍已被广泛研究，通过amp激活的蛋白激酶激活、哺乳动物雷帕霉素抑制靶点和减少胰岛素样生长因子1信号传导显示抗癌特性。胰高血糖素样肽-1受体激动剂，包括西马鲁肽和替西肽，可促进体重减轻、胰岛素敏感性和抗炎作用，新出现的证据表明其具有直接的肿瘤抑制作用。钠-葡萄糖共转运蛋白2抑制剂通过降低葡萄糖可用性和减轻全身炎症来调节肿瘤代谢。其他药物，包括二肽基肽酶-4抑制剂、噻唑烷二酮类、磺脲类和α -葡萄糖苷酶抑制剂，已显示出其潜在抗癌作用的混合证据，需要进一步研究。虽然观察性研究和荟萃分析表明，某些抗糖尿病和抗肥胖药物可能降低癌症风险，但专门评估癌症预防的随机对照试验有限。此外，长期的安全性问题，包括在特定情况下潜在的促肿瘤作用，值得进一步研究。未来的研究应该集中在大规模的临床试验和机制研究上，以验证这些药物的肿瘤益处和风险。

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引用次数: 0

The role of deiodinases on metabolic alteration in cancer 脱碘酶在癌症代谢改变中的作用。

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-07-10 DOI: 10.1016/j.semcancer.2025.07.003

Caterina Miro , Annunziata Gaetana Cicatiello , Monica Dentice , Annarita Nappi

Deiodinases are key regulators of Thyroid Hormone (TH) bioavailability, exerting a precise spatial and temporal control over T3 levels in peripheral tissues. By dynamically modulating TH activation and inactivation, deiodinases allow target organs to adapt TH signaling to physiological and pathological demands, highlighting their importance in both health and disease. In cancer, their dysregulated expression reprograms cellular metabolism and shapes the tumor microenvironment (TME). Type 3 deiodinase (D3), frequently upregulated in proliferative and hypoxic tumor regions, fosters cell proliferation and resistance to differentiation. Conversely, type 2 deiodinase (D2) sustains glycolytic metabolism, angiogenesis, and redox disbalance, particularly in aggressive and p53-deficient tumors. Beyond cancer cells, deiodinases activity influences stromal and immune compartments, impacting glutamine metabolism and immune cell plasticity. This complex endocrine-metabolic axis supports tumor adaptation to stress and contributes to the emergence of resistance to therapy. Recent advances reveal the potential of targeting deiodinases to counteract cancer metabolic reprogramming and re-sensitize tumors to treatment. Given the essential and multifaceted roles of deiodinases in cancer biology, a comprehensive understanding of their mechanisms of action, regulation, and clinical implications is critical. This review aims to summarize current knowledge on the roles of deiodinases in cancer metabolism and immunity, focusing on their biochemical properties, regulatory networks, tissue-specific functions, and contributions to disease. In doing so, we seek to highlight emerging concepts in local TH signaling and explore potential avenues for therapeutic intervention targeting deiodinase pathways in precision oncology.

脱碘酶是甲状腺激素（TH）生物利用度的关键调节因子，对外周组织中T3水平施加精确的时空控制。通过动态调节TH的激活和失活，脱碘酶允许目标器官适应生理和病理需求的TH信号，突出了它们在健康和疾病中的重要性。在癌症中，它们的失调表达重编程细胞代谢并塑造肿瘤微环境（TME）。3型脱碘酶（D3），在增殖和缺氧肿瘤区域经常上调，促进细胞增殖和分化抵抗。相反，2型脱碘酶（D2）维持糖酵解代谢、血管生成和氧化还原失衡，特别是在侵袭性和p53缺乏的肿瘤中。除癌细胞外，脱碘酶活性还影响基质和免疫室，影响谷氨酰胺代谢和免疫细胞的可塑性。这种复杂的内分泌代谢轴支持肿瘤对压力的适应，并有助于对治疗产生耐药性。最近的进展揭示了靶向去碘酶对抗癌症代谢重编程和使肿瘤对治疗再敏感的潜力。鉴于脱碘酶在癌症生物学中的重要和多方面的作用，全面了解它们的作用机制、调节和临床意义是至关重要的。本文综述了脱碘酶在肿瘤代谢和免疫中的作用，重点介绍了它们的生化特性、调节网络、组织特异性功能和对疾病的贡献。在此过程中，我们试图突出局部TH信号的新兴概念，并探索精准肿瘤学中针对脱碘酶途径的治疗干预的潜在途径。

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引用次数: 0

CRISPR/Cas9 genome engineering in PDAC: From preclinical studies to translation and clinical research PDAC中的CRISPR/Cas9基因组工程：从临床前研究到翻译和临床研究

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-07-10 DOI: 10.1016/j.semcancer.2025.07.004

Yanxi Lu , Jojanneke Stoof , Yaba Rosette Tanoé , Naomi Walsh , Maarten F. Bijlsma , Huijun Lei , Tianhui Chen , Jelena Grahovac , Robert Grützmann , Christian Pilarsky

CRISPR/Cas9 technology has emerged as a powerful tool in pancreatic ductal adenocarcinoma cancer (PDAC) research, facilitating the study of genes involved in cell signaling pathways, proliferation, migration, invasion, and chemotherapy resistance. In this review, we discuss the evolution of CRISPR technologies from sophisticated editing techniques to broad screening methods, examine the utility of isogenic models and genetically engineered mouse models (GEMMs). We also explore how CRISPR/Cas9 screens can reveal immune-tumor cell interactions, highlighting the multifaceted role of this technology in PDAC research. Moreover, we emphasize the use of CRISPR technology in diagnostics for CAR-T cell therapies, where CRISPR/Cas9 enhances the precision of targeting malignant cells while minimizing off-tumor effects.

CRISPR/Cas9技术已成为胰腺导管腺癌（pancreatic ductal adenocarcinoma cancer， PDAC）研究的有力工具，促进了对细胞信号通路、增殖、迁移、侵袭、化疗耐药等相关基因的研究。在这篇综述中，我们讨论了CRISPR技术从复杂的编辑技术到广泛的筛选方法的演变，研究了等基因模型和基因工程小鼠模型（GEMMs）的实用性。我们还探讨了CRISPR/Cas9筛选如何揭示免疫肿瘤细胞相互作用，突出了该技术在PDAC研究中的多方面作用。此外，我们强调在CAR-T细胞治疗的诊断中使用CRISPR技术，其中CRISPR/Cas9提高了靶向恶性细胞的精度，同时最大限度地减少了非肿瘤效应。

引用次数: 0

The impact of sarcopenic obesity on cancer clinical outcomes 肌肉减少型肥胖对癌症临床结果的影响

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-07-08 DOI: 10.1016/j.semcancer.2025.07.002

Bahadır Köylü , Cem Sulu , Volkan Demirhan Yumuk , Perran Fulden Yumuk

Sarcopenic obesity is a distinct clinical condition characterized by the coexistence of excess fat and reduced muscle mass. Although the prevalence of sarcopenic obesity varies depending on the definition used, it is increasingly recognized as a significant health concern, regardless of age and underlying disease. Despite limited understanding of the crosstalk between sarcopenic obesity and cancer, emerging evidence suggests that sarcopenic obesity not only promotes a metabolic and inflammatory environment conducive to cancer progression but also profoundly impacts treatment efficacy, safety, and survival outcomes. This review provides a concise overview of the key aspects of sarcopenic obesity, with a particular focus on its role in the cancer setting. We also assess existing evidence on its influence on oncological outcomes in both early and advanced stages of the various solid tumor types.

肌少性肥胖是一种独特的临床病症，其特征是脂肪过多和肌肉质量减少并存。尽管肌少性肥胖的流行程度因使用的定义而异，但它越来越被认为是一个重要的健康问题，与年龄和潜在疾病无关。尽管对肌少性肥胖和癌症之间的相互关系了解有限，但新出现的证据表明，肌少性肥胖不仅促进了有利于癌症进展的代谢和炎症环境，而且深刻影响了治疗的有效性、安全性和生存结果。这篇综述简要概述了肌肉减少性肥胖的关键方面，特别关注其在癌症环境中的作用。我们还评估了其对各种实体瘤类型早期和晚期肿瘤预后影响的现有证据。

引用次数: 0

From awareness to action: Revolutionizing cardio-oncology in China 从意识到行动：革新中国的心脏肿瘤学

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-07-07 DOI: 10.1016/j.semcancer.2025.06.011

Aman Wang, Jiwei Liu

Cardio-oncology is an emerging interdisciplinary field focused on the intersection of cancer and cardiovascular disease. With the rising incidence of both cancer and cardiovascular disease in China, establishing a strong cardio-oncology framework has become essential. This review examines the historical development, clinical practices, and key milestones of cardio-oncology in China, emphasizing the importance of multidisciplinary teams, specialized guidelines, and international collaborations. Additionally, it discusses the current challenges and future opportunities for advancing cardio-oncology within China’s healthcare landscape.

心脏肿瘤学是一个新兴的跨学科领域，专注于癌症和心血管疾病的交叉。随着中国癌症和心血管疾病的发病率不断上升，建立一个强有力的心脏肿瘤学框架已变得至关重要。本文回顾了中国心脏肿瘤学的历史发展、临床实践和关键里程碑，强调了多学科团队、专业指南和国际合作的重要性。此外，它还讨论了在中国医疗保健领域推进心脏肿瘤学的当前挑战和未来机遇。

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Reopening Pandora’s box: Is there a role for HDL in breast cancer? 重新打开潘多拉的盒子：高密度脂蛋白在乳腺癌中有作用吗？

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-07-05 DOI: 10.1016/j.semcancer.2025.07.001

Maria Isabela Bloise Alves Caldas Sawada , Monique de Fatima de Mello Santana , Milena Gomes Vancini , Marisa Passarelli

Plasma lipid and lipoprotein profiles are recognized as key modulators in breast cancer (BC) development. Notably, the association between high-density lipoprotein cholesterol (HDLc) and BC remains controversial, with studies reporting positive, negative, or no correlation. This inconsistency may arise from the clinical metrics used to quantify high-density lipoproteins (HDL), such as HDLc and apolipoprotein (apo) A-1, which may not accurately reflect HDL functionality in modulating the tumor microenvironment. Moreover, HDL particles isolated from plasma may undergo modifications influenced by tumor activity, varying with disease stage, severity, and treatment. In this review, we are critically reopening Pandora´s box analyzing evidence on HDLc plasma levels and HDL functionality in BC. Specifically, HDL contributes to tumor regulation by removing excess cellular cholesterol, thereby limiting sterol availability for cell replication and metastasis. Additionally, HDL exerts antioxidant and anti-inflammatory effects and acts as a carrier of bioactive proteins, lipids, and microRNAs, facilitating their delivery to target cells and modulating intracellular signaling and gene expression. Collectively, HDL functionality may serve as a predictor of therapeutic response and clinical outcomes in BC.

血浆脂质和脂蛋白谱被认为是乳腺癌（BC）发展的关键调节因子。值得注意的是，高密度脂蛋白胆固醇（HDLc）与BC之间的关系仍然存在争议，研究报告呈正相关、负相关或无相关。这种不一致可能是由于用于量化高密度脂蛋白（HDL）的临床指标，如HDL和载脂蛋白A-1，可能不能准确反映HDL在调节肿瘤微环境中的功能。此外，从血浆中分离出的HDL颗粒可能受到肿瘤活性的影响，随疾病分期、严重程度和治疗而变化。在这篇综述中，我们重新打开潘多拉的盒子，分析BC患者HDL血浆水平和HDL功能的证据。具体来说，HDL通过去除多余的细胞胆固醇来调节肿瘤，从而限制了细胞复制和转移的固醇可用性。此外，HDL具有抗氧化和抗炎作用，并作为生物活性蛋白、脂质和microrna的载体，促进其递送到靶细胞并调节细胞内信号传导和基因表达。总的来说，HDL功能可以作为BC治疗反应和临床结果的预测因子。

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引用次数: 0

Advances and mechanisms of gut microbiota modulation in enhancing immune checkpoint inhibitor efficacy 肠道菌群调节增强免疫检查点抑制剂疗效的研究进展及机制。

IF 12.1 1区医学 Q1 ONCOLOGY

Seminars in cancer biology

Pub Date : 2025-07-03 DOI: 10.1016/j.semcancer.2025.06.012

Li Chen , Baoyi Li , Menghang Zu , Rui L. Reis , Subhas C. Kundu , Bo Xiao

The gut microbiota is crucial for maintaining human health by regulating immune homeostasis and metabolic function. Immune checkpoint inhibitors (ICIs) have emerged as a cornerstone of cancer immunotherapy, yet their effectiveness is often hampered by treatment resistance and immune-related adverse events (irAEs). Increasing evidence highlights gut microbiota as a critical determinant of ICI efficacy. Here, we summarize the advances from preclinical mouse models and clinical trials to systematically illustrate how gut microbiota modulation strategies, such as fecal microbiota transplantation, specific microorganism supplementation, dietary and lifestyle interventions, and prebiotic/postbiotic supplementation, can enhance ICI therapeutic outcomes and mitigate irAEs. Mechanistically, the gut microbiota shape host immune responses, influencing innate, adaptive, and mucosal immunity, as well as immune checkpoint expression, through microbial translocation, microbiota-derived metabolites, and extracellular vesicles. This review elucidates the intricate interplay between gut microbiota and ICI treatment responses, laying a theoretical groundwork for developing personalized microbiota-based strategies to optimize cancer immunotherapy.

肠道菌群通过调节免疫稳态和代谢功能，对维持人体健康至关重要。免疫检查点抑制剂（ICIs）已成为癌症免疫治疗的基石，但其有效性往往受到治疗耐药性和免疫相关不良事件（irAEs）的阻碍。越来越多的证据表明，肠道微生物群是ICI疗效的关键决定因素。在这里，我们总结了临床前小鼠模型和临床试验的进展，以系统地说明肠道微生物群调节策略，如粪便微生物群移植、特定微生物补充、饮食和生活方式干预以及益生元/益生后补充，如何提高ICI治疗效果并减轻irAEs。从机制上讲，肠道微生物群通过微生物易位、微生物群衍生代谢物和细胞外囊泡塑造宿主免疫反应，影响先天免疫、适应性免疫和粘膜免疫，以及免疫检查点表达。这篇综述阐明了肠道微生物群与ICI治疗反应之间复杂的相互作用，为开发个性化的基于微生物群的策略来优化癌症免疫治疗奠定了理论基础。

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引用次数: 0