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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 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 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 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 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。
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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 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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引用次数: 0
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 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
Epithelial-mesenchymal transition promotes metabolic reprogramming to suppress ferroptosis 上皮-间质转化促进代谢重编程抑制铁下垂。
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-07-01 Epub Date: 2025-03-07 DOI: 10.1016/j.semcancer.2025.02.013
Wenzheng Guo, Zhibing Duan, Jingjing Wu, Binhua P. Zhou
Epithelial-mesenchymal transition (EMT) is a cellular de-differentiation process that provides cells with the increased plasticity and stem cell-like traits required during embryonic development, tissue remodeling, wound healing and metastasis. Morphologically, EMT confers tumor cells with fibroblast-like properties that lead to the rearrangement of cytoskeleton (loss of stiffness) and decrease of membrane rigidity by incorporating high level of poly-unsaturated fatty acids (PUFA) in their phospholipid membrane. Although large amounts of PUFA in membrane reduces rigidity and offers capabilities for tumor cells with the unbridled ability to stretch, bend and twist in metastasis, these PUFA are highly susceptible to lipid peroxidation, which leads to the breakdown of membrane integrity and, ultimately results in ferroptosis. To escape the ferroptotic risk, EMT also triggers the rewiring of metabolic program, particularly in lipid metabolism, to enforce the epigenetic regulation of EMT and mitigate the potential damages from ferroptosis. Thus, the interplay among EMT, lipid metabolism, and ferroptosis highlights a new layer of intricated regulation in cancer biology and metastasis. Here we summarize the latest findings and discuss these mutual interactions. Finally, we provide perspectives of how these interplays contribute to cellular plasticity and ferroptosis resistance in metastatic tumor cells that can be explored for innovative therapeutic interventions.
上皮间充质转化(Epithelial-mesenchymal transition, EMT)是一个细胞去分化的过程,它为细胞提供了胚胎发育、组织重塑、伤口愈合和转移所需的可塑性和干细胞样特征。形态学上,EMT使肿瘤细胞具有成纤维细胞样特性,通过在其磷脂膜中加入高水平的多不饱和脂肪酸(PUFA),导致细胞骨架重排(刚度丧失)和膜刚度降低。尽管膜中大量的PUFA降低了刚性,并为肿瘤细胞在转移过程中提供了无限制的拉伸、弯曲和扭曲的能力,但这些PUFA极易受到脂质过氧化的影响,从而导致膜完整性的破坏,最终导致铁下垂。为了避免铁下垂风险,EMT还触发代谢程序的重新布线,特别是在脂质代谢中,以加强EMT的表观遗传调控,减轻铁下垂的潜在损害。因此,EMT、脂质代谢和铁下垂之间的相互作用突出了癌症生物学和转移中复杂调控的新层面。在这里,我们总结了最新的发现,并讨论了这些相互作用。最后,我们提供了这些相互作用如何促进转移性肿瘤细胞的细胞可塑性和铁下垂抵抗的观点,可以探索创新的治疗干预措施。
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引用次数: 0
The impact of the tumor microenvironment in the dual burden of obesity-cancer link 肿瘤微环境在肥胖-癌症双重负担中的影响。
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-07-01 Epub Date: 2025-03-22 DOI: 10.1016/j.semcancer.2025.03.001
Serena Sagliocchi , Lucia Acampora , Biagio Barone , Felice Crocetto , Monica Dentice
Obesity induces systemic perturbations of tissue homeostasis, leading to dyslipidemia, insulin resistance and chronic state of inflammation. Evidence from clinical and preclinical studies links excess of adiposity with increased cancer incidence and suggests that chronic inflammation may contribute to increased cancer risk in obese patients. Over the last decades of obesity research, multifaced and complicated effects of abnormal or excessive expansion of Adipose Tissue have been uncovered. In particular, it is widely described how obesity can exacerbate the tumorigenesis for instance by fueling soluble signals and adipokines and by enhancing tissue inflammation and altering the hormonal balance. Less is known about the paracrine effects of the cancer-associated adipocytes on the tumor cells and still poorly explored is the reciprocal communication between cancer cells and the adipose component of the tumor microenvironment (TME). In this review, we will address the mechanisms by which the peritumoral Adipose Tissue can influence the dynamics of tumoral cells. We will discuss how obesity-induced changes in the tumor microenvironment may enhance tumor growth and aggressive characteristics leading to increased invasiveness and metastatic progression of cancer that leads to a worsen cancer survival in obese subjects. We conclude that targeting the peritumoral adipose component of the TME would be a therapeutic option to prevent cancer development.
肥胖引起全身组织稳态紊乱,导致血脂异常、胰岛素抵抗和慢性炎症状态。来自临床和临床前研究的证据表明,过度肥胖与癌症发病率增加有关,并表明慢性炎症可能会增加肥胖患者患癌症的风险。在过去几十年的肥胖研究中,发现了脂肪组织异常或过度扩张的多方面和复杂的影响。特别是,人们广泛地描述了肥胖如何加剧肿瘤的发生,例如,通过增加可溶性信号和脂肪因子,通过增强组织炎症和改变激素平衡。癌症相关脂肪细胞对肿瘤细胞的旁分泌作用尚不清楚,癌细胞与肿瘤微环境(TME)中脂肪成分之间的相互交流仍未得到充分探讨。在这篇综述中,我们将讨论肿瘤周围脂肪组织影响肿瘤细胞动力学的机制。我们将讨论肥胖诱导的肿瘤微环境变化如何促进肿瘤生长和侵袭性特征,从而增加癌症的侵袭性和转移性进展,从而导致肥胖受试者癌症生存恶化。我们的结论是,针对肿瘤周围的脂肪成分的TME将是一个治疗选择,以防止癌症的发展。
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引用次数: 0
Cathepsins: Emerging targets in the tumor ecosystem to overcome cancers 组织蛋白酶:肿瘤生态系统中克服癌症的新靶点
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-07-01 Epub Date: 2025-04-12 DOI: 10.1016/j.semcancer.2025.04.001
Yuki Fujii , Zahra Asadi , Kamiya Mehla
Cathepsins, a group of lysosomal peptidases, have traditionally been recognized as tumor facilitators. Recent research, however, highlights their critical role in orchestrating cancer and the tumor microenvironment (TME). Primality, cathepsins degrade extracellular matrix, enabling cancer cells to invade and metastasize, while also promoting vascular endothelial infiltration and subsequent angiogenesis. Additionally, cathepsins boost fibroblast growth, thereby supporting tumor progression. More importantly, cathepsins are pivotal in modulating immune cells within the TME by regulating their recruitment, antigen processing and presentation, differentiation, and cell death, primarily contributing to immune suppression. Given their overexpression in tumors and elevated levels in the circulation of cancer patients, it is crucial to consider the systemic effects of cathepsins. Although the comprehensive role of cathepsins in cancer patients’ bodies remains underexplored, they likely influence systemic immunity and inflammation, cellular metabolism, muscle wasting, and distant metastasis through their unique proteolytic functions. Notably, cathepsins also confer resistance to chemoradiotherapy by rewriting the cellular profile within the TME. In this context, promising results are emerging from studies combining cathepsin inhibitors with conventional therapies to suppress tumor development effectively. This review aims to decipher the cathepsin-driven networks within cancer cells and the TME, detailing their contribution to chemoradioresistance by reshaping both micro- and macroenvironments. Furthermore, we explore current and future perspectives on therapies targeting cathepsins’ interactions, offering insights into innovative treatment strategies.
组织蛋白酶是一组溶酶体肽酶,传统上被认为是肿瘤促进剂。然而,最近的研究强调了它们在协调癌症和肿瘤微环境(TME)中的关键作用。首先,组织蛋白酶降解细胞外基质,使癌细胞侵袭和转移,同时也促进血管内皮浸润和随后的血管生成。此外,组织蛋白酶促进成纤维细胞生长,从而支持肿瘤进展。更重要的是,组织蛋白酶通过调节TME内的免疫细胞募集、抗原加工和递呈、分化和细胞死亡,在调节免疫细胞方面起着关键作用,主要有助于免疫抑制。考虑到组织蛋白酶在肿瘤中的过度表达和癌症患者血液循环中的水平升高,考虑组织蛋白酶的全身作用是至关重要的。尽管组织蛋白酶在癌症患者体内的全面作用尚未得到充分研究,但它们可能通过其独特的蛋白水解功能影响全身免疫和炎症、细胞代谢、肌肉萎缩和远处转移。值得注意的是,组织蛋白酶还通过重写TME内的细胞谱来赋予对放化疗的耐药性。在这种背景下,将组织蛋白酶抑制剂与常规疗法结合起来有效抑制肿瘤发展的研究正在出现有希望的结果。本综述旨在解读癌细胞和TME内组织蛋白酶驱动的网络,详细介绍它们通过重塑微观和宏观环境对放化疗耐药的贡献。此外,我们探讨了当前和未来针对组织蛋白酶相互作用的治疗观点,为创新治疗策略提供见解。
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引用次数: 0
Navigating the weight: The impact of obesity on gastrointestinal cancer surgery and strategies for improved outcomes 导航体重:肥胖对胃肠癌手术的影响和改善结果的策略
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-06-26 DOI: 10.1016/j.semcancer.2025.06.010
Gerardo Sarno , Claudia Reytor-González , Evelyn Frias-Toral , Martín Campuzano-Donoso , Christos S. Katsanos , Daniel Simancas-Racines
Obesity significantly affects gastrointestinal cancer surgery outcomes by creating complex challenges throughout the preoperative, intraoperative, and postoperative stages. This narrative review explores the intricate relationship between obesity and GIC surgery, highlighting the dual burden of obesity as a global public health issue and a determinant of surgical complications. The review aims to analyze physiological and technical hurdles, including limited visibility, prolonged operative times, increased perioperative risks, and adverse recovery outcomes associated with obesity. Evidence emphasizes the critical role of excess visceral fat, systemic inflammation, and insulin resistance in elevating surgical risks. Mitigation strategies involve preoperative nutritional optimization, use of advanced surgical technologies such as robotic-assisted and laparoscopic systems, and individualized postoperative care, encompassing early mobilization, tailored pain management, and close monitoring of metabolic parameters. Despite advancements, knowledge gaps remain, particularly regarding sarcopenic obesity and the long-term impact of preoperative dietary interventions. Future research should focus on refining minimally invasive techniques, integrating personalized medicine, and exploring innovative perioperative protocols to address obesity-related risks effectively. By fostering a multidisciplinary approach, this review underscores the necessity for targeted interventions to enhance outcomes and improve the quality of care for patients with obesity undergoing gastrointestinal cancer surgery.
肥胖通过在术前、术中和术后阶段制造复杂的挑战,显著影响胃肠道肿瘤手术结果。这篇叙述性综述探讨了肥胖和GIC手术之间的复杂关系,强调了肥胖作为全球公共卫生问题和手术并发症决定因素的双重负担。该综述旨在分析与肥胖相关的生理和技术障碍,包括能见度有限、手术时间延长、围手术期风险增加和不良恢复结果。证据强调内脏脂肪过多、全身性炎症和胰岛素抵抗在增加手术风险中的关键作用。缓解策略包括术前营养优化,使用先进的手术技术,如机器人辅助和腹腔镜系统,以及个性化的术后护理,包括早期活动,量身定制的疼痛管理和密切监测代谢参数。尽管取得了进展,但知识差距仍然存在,特别是关于肌肉减少性肥胖和术前饮食干预的长期影响。未来的研究应侧重于改进微创技术,整合个性化医疗,探索创新的围手术期方案,以有效解决肥胖相关风险。通过培养多学科的方法,本综述强调有针对性的干预措施的必要性,以提高结果和改善治疗质量的肥胖患者接受胃肠道肿瘤手术。
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引用次数: 0
The microbiome-immune cell interaction network: Advancing tumor immunotherapy 微生物组-免疫细胞相互作用网络:推进肿瘤免疫治疗
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-06-24 DOI: 10.1016/j.semcancer.2025.06.009
Wei Liu, Zhou Lan, Zhenzi Lin, Yuyue Zhao, Junxiang Lian, Guangtao Yu
Tumor immunotherapy has achieved revolutionary advancements; however, owing to the complex interplay of multiple intrinsic and extrinsic tumor factors, the patient response rate remains suboptimal. Recent research has emphasized the pivotal role of microbiome in tumor progression. Under normal physiological conditions, microbiome enter orally and colonize sites such as the oral and intestinal mucosa, establishing a dynamic microbiome equilibrium that participates in essential physiological processes, including host metabolism and immune regulation. However, in pathological states, including dysbiosis, tumor initiation, or compromised mucosal barrier function, the microbiome can penetrate the mucosal barrier, infiltrate tumor tissues, and engage in intricate direct or indirect interactions with immune cells. These interactions play a pivotal role in reshaping the tumor immune microenvironment and modulating the host's anti-tumor immune response. This review elaborate the regulatory mechanisms involved in direct and indirect interactions between microbiome and immune cells within tumors, and their implications for tumor immunotherapy. We discuss the external factors that impact these interactions and outline the potential use of engineered bacteria in cancer treatment. From the perspective of the interaction network between microbiomes and immune cells, this review elucidates the mechanisms and potential of microbiomes in tumor immunotherapy, offering new insights and potential targets for innovative strategies in tumor prevention and treatment.
肿瘤免疫治疗取得革命性进展;然而,由于多种内在和外在肿瘤因素的复杂相互作用,患者的反应率仍然不理想。最近的研究强调了微生物组在肿瘤进展中的关键作用。在正常生理条件下,微生物组通过口腔进入机体并定植于口腔和肠道粘膜等部位,形成动态的微生物组平衡,参与机体代谢和免疫调节等重要生理过程。然而,在病理状态下,包括生态失调、肿瘤起始或粘膜屏障功能受损,微生物组可以穿透粘膜屏障,浸润肿瘤组织,并与免疫细胞进行复杂的直接或间接相互作用。这些相互作用在重塑肿瘤免疫微环境和调节宿主抗肿瘤免疫反应中起着关键作用。本文综述了肿瘤内微生物群与免疫细胞直接和间接相互作用的调控机制及其对肿瘤免疫治疗的启示。我们讨论了影响这些相互作用的外部因素,并概述了工程细菌在癌症治疗中的潜在用途。本文从微生物组与免疫细胞相互作用网络的角度,阐述微生物组在肿瘤免疫治疗中的作用机制和潜力,为肿瘤预防和治疗的创新策略提供新的见解和潜在的靶点。
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引用次数: 0
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Seminars in cancer biology
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