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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
Lipids and lipoproteins in the interstitial tissue fluid regulate the formation of dysfunctional tissue-resident macrophages: Implications for atherogenic, tumorigenic, and obesogenic processes 间质组织液中的脂质和脂蛋白调节功能失调的组织巨噬细胞的形成:与动脉粥样硬化、致瘤性和致肥过程的关系。
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-06-20 DOI: 10.1016/j.semcancer.2025.06.008
Miriam Lee-Rueckert , Matti Jauhiainen , Petri T. Kovanen , Joan Carles Escolà-Gil
An inflammatory and lipid-enriched tissue microenvironment is a common characteristic of the extracellular niches of affected tissues in atherosclerosis, cancer, and obesity. These respective interstitial environments appear to be induced by infiltration of plasma lipids and early local recruitment of monocyte-derived macrophages. In the tissue niches, the macrophages display remarkable phenotypic and functional plasticity and exert multifaceted roles in tissue homeostasis. Multiple local signaling events contribute to the phenotypic polarization of the tissue-resident macrophages into M1-like, M2-like, and multiple mixed subpopulations. This study aims to review and compare the roles of lipids and lipoproteins in shaping the inflammatory and lipid-enriched microenvironments of atherosclerotic arterial intima, malignant tumors, and obese adipose tissue, so generating dysfunctional macrophages. Circulating lipoprotein-bound lipids and albumin-bound fatty acids can cross the vascular endothelial barrier and infiltrate the interstitial fluids, resulting in variable levels of plasma-derived lipids, notably low-density lipoproteins (LDL), high-density lipoproteins (HDL), and locally generated small lipid-poor HDL species (preβ-HDL). Whilst LDL particles mainly supply liver-derived cholesterol to the cells of peripheral tissues, HDL particles can promote the reverse transfer of cellular cholesterol into the circulation and ultimately via the liver to the gut for its fecal excretion. Thus, the LDL/HDL ratio in the interstitial fluids can either promote or prevent cholesterol accumulation in the tissue-resident macrophages. Various types of peripheral cells modify interstitial LDL and HDL particles by oxidation, proteolysis, lipolysis, aggregation, or fusion, rendering them dysfunctional. By engulfing excessive amounts of extracellular lipids and modified LDL particles in such lipid-rich microenvironments, macrophages can become dysfunctional, a typical example being the atherosclerotic arterial intima. Similarly, tissue microenvironments characteristic of several malignant tumors and the obese adipose tissue are rich in triglyceride (TG)-rich lipoproteins and free fatty acids, inducing accumulation of TG and glycerophospholipids in the intracellular lipid droplets of macrophages. The lipid-loaded macrophages are currently considered novel markers for diagnosis and selective therapeutic targets not only in the arterial intima but also in malignant tumors and obese adipose tissue. Together, the available data identify potential roles of lipids and lipoproteins present in the interstitial fluids of the atherosclerotic arterial intima, malignant tumors, and obese adipose tissue in the generation of distinct lipid-loaded macrophage subpopulations and suggest their contributory roles in the development and progression of atherosclerosis, cancer, and obesity, the three major health concerns worldwide.
炎症和富含脂质的组织微环境是动脉粥样硬化、癌症和肥胖症中受影响组织的细胞外生态位的共同特征。这些不同的间质环境似乎是由血浆脂质浸润和单核细胞源性巨噬细胞的早期局部募集诱导的。在组织壁龛中,巨噬细胞表现出显著的表型和功能可塑性,并在组织稳态中发挥多方面的作用。多个局部信号事件导致组织内巨噬细胞表型分化为m1样、m2样和多个混合亚群。本研究旨在回顾和比较脂质和脂蛋白在形成动脉粥样硬化内膜、恶性肿瘤和肥胖脂肪组织的炎症和富含脂质的微环境,从而产生功能失调的巨噬细胞中的作用。循环脂蛋白结合的脂质和白蛋白结合的脂肪酸可以穿过血管内皮屏障并浸润间质液,导致血浆来源的脂质水平变化,特别是低密度脂蛋白(LDL)、高密度脂蛋白(HDL)和局部生成的小脂质贫HDL物种(前β-HDL)。LDL颗粒主要向外周组织细胞提供肝源性胆固醇,而HDL颗粒可以促进细胞胆固醇逆向转移进入循环,最终通过肝脏进入肠道粪便排泄。因此,间质液中的LDL/HDL比值可以促进或阻止组织内巨噬细胞中的胆固醇积累。各种类型的外周细胞通过氧化、蛋白水解、脂解、聚集或融合改变间质LDL和HDL颗粒,使其功能失调。在这种富含脂质的微环境中,巨噬细胞通过吞噬过量的细胞外脂质和修饰的LDL颗粒而变得功能失调,典型的例子是动脉粥样硬化的动脉内膜。同样,一些恶性肿瘤和肥胖脂肪组织的组织微环境也富含富含甘油三酯(TG)的脂蛋白和游离脂肪酸,从而诱导巨噬细胞内脂滴中TG和甘油磷脂的积累。脂质巨噬细胞不仅在动脉内膜,而且在恶性肿瘤和肥胖脂肪组织中都被认为是诊断和选择性治疗的新标志物。总之,现有数据确定了存在于动脉粥样硬化动脉内膜、恶性肿瘤和肥胖脂肪组织的间质液中的脂质和脂蛋白在产生不同的脂质负载巨噬细胞亚群中的潜在作用,并表明它们在动脉粥样硬化、癌症和肥胖这三大全球健康问题的发生和进展中所起的促进作用。
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引用次数: 0
Nutrient acquisition of gut microbiota: Implications for tumor immunity 肠道微生物群的营养获取:对肿瘤免疫的影响。
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-06-13 DOI: 10.1016/j.semcancer.2025.06.003
Yusha Wang , Jing Huang , Huan Tong , Yuting Jiang , Yu Jiang , Xuelei Ma
The gut microbiota is essential in colorectal cancer (CRC) development, progression, and therapeutic responsiveness through its metabolic acquisitions and immunomodulatory functions. The composition of gut microbiota is shaped by habitat filters such as oxygen availability, dietary components, and host-derived factors, which influence both bacterial colonization and metabolic strategies. Furthermore, microbial metabolism of carbohydrates, proteins, and lipids produces metabolites, including short-chain fatty acids (SCFAs), polyamines, ammonia, hydrogen sulfide, and secondary bile acids (BAs). These microbial metabolites can either support anti-tumor immune surveillance or promote tumorigenesis depending on their type, concentration, and the host context. Consequently, interventions such as high-fiber diets, prebiotic and probiotic supplementation, and fecal microbiota transplantation (FMT) have emerged as promising strategies to reshape the gut ecosystem and improve CRC treatment efficacy. This review summarizes current insights into microbial nutrient metabolism, discusses the immune-regulatory effects of key microbial metabolites, and explores microbiota-targeted strategies for enhancing antitumor efficacy. Understanding these interactions offers new therapeutic opportunities for cancer prevention and treatment.
肠道微生物群通过其代谢获取和免疫调节功能在结直肠癌(CRC)的发生、进展和治疗反应中至关重要。肠道菌群的组成受到栖息地过滤器的影响,如氧气利用率、饮食成分和宿主来源的因素,这些因素影响细菌的定植和代谢策略。此外,碳水化合物、蛋白质和脂质的微生物代谢产生代谢物,包括短链脂肪酸(SCFAs)、多胺、氨、硫化氢和次级胆汁酸(BAs)。这些微生物代谢物既可以支持抗肿瘤免疫监视,也可以促进肿瘤发生,这取决于它们的类型、浓度和宿主环境。因此,高纤维饮食、益生元和益生菌补充以及粪便微生物群移植(FMT)等干预措施已成为重塑肠道生态系统和提高结直肠癌治疗效果的有希望的策略。本文综述了微生物营养代谢的最新研究成果,讨论了关键微生物代谢物的免疫调节作用,并探讨了以微生物群为靶点的抗肿瘤策略。了解这些相互作用为癌症的预防和治疗提供了新的治疗机会。
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引用次数: 0
Thematic issue: Obesity-driven cancer: Clinical and molecular aspects 专题问题:肥胖驱动的癌症:临床和分子方面。
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-06-13 DOI: 10.1016/j.semcancer.2025.06.006
Emmanuel Jacobo-Tovar, Andrea Medel-Sánchez, Cosette Durán-Castillo, Rodolfo Guardado-Mendoza
Obesity-associated insulin resistance (IR) is characterized by a chronic low-grade inflammatory state driven by adipocyte dysfunction, elevated free fatty acids, and proinflammatory cytokines. These factors activate signaling pathways—including JNK, TLR, and NF-κB—that impair insulin receptor function and promote hyperinsulinemia. Elevated insulin reduces insulin-like growth factor binding proteins, thereby increasing the bioavailability of IGF-1 and IGF-2, which stimulate oncogenic pathways such as PI3K-AKT-mTOR and RAS-MAPK. Epidemiological evidence links IR to an increased risk of a broad spectrum of malignancies, though associations vary by cancer subtype, patient demographics, and tumor characteristics. Therapeutic strategies targeting IR—ranging from lifestyle interventions and weight reduction to pharmacological agents like metformin and GLP-1 receptor agonists—have shown promise in reducing cancer risk and improving prognosis. Metformin exhibits anticancer effects through both AMPK-dependent and independent mechanisms, including mTOR inhibition, suppression of cell proliferation, and attenuation of oxidative stress. While observational studies support a relationship between improved insulin sensitivity and reduced cancer risk, definitive evidence from interventional trials remains limited. Overall, these findings underscore the critical role of metabolic dysfunction in tumorigenesis and highlight the potential of IR-targeted therapies in cancer prevention and management.
肥胖相关胰岛素抵抗(IR)的特征是由脂肪细胞功能障碍、游离脂肪酸升高和促炎细胞因子驱动的慢性低度炎症状态。这些因子激活包括JNK、TLR和NF-κ b在内的信号通路,损害胰岛素受体功能并促进高胰岛素血症。胰岛素升高会降低胰岛素样生长因子结合蛋白,从而增加IGF-1和IGF-2的生物利用度,从而刺激PI3K-AKT-mTOR和RAS-MAPK等致癌途径。流行病学证据表明,IR与多种恶性肿瘤的风险增加有关,尽管相关关系因癌症亚型、患者人口统计学和肿瘤特征而异。针对ir的治疗策略-从生活方式干预和减肥到像二甲双胍和GLP-1受体激动剂这样的药理学药物-已经显示出降低癌症风险和改善预后的希望。二甲双胍通过ampk依赖性和独立机制显示抗癌作用,包括mTOR抑制、细胞增殖抑制和氧化应激衰减。虽然观察性研究支持改善胰岛素敏感性和降低癌症风险之间的关系,但来自介入性试验的明确证据仍然有限。总的来说,这些发现强调了代谢功能障碍在肿瘤发生中的关键作用,并强调了ir靶向治疗在癌症预防和治疗中的潜力。
{"title":"Thematic issue: Obesity-driven cancer: Clinical and molecular aspects","authors":"Emmanuel Jacobo-Tovar,&nbsp;Andrea Medel-Sánchez,&nbsp;Cosette Durán-Castillo,&nbsp;Rodolfo Guardado-Mendoza","doi":"10.1016/j.semcancer.2025.06.006","DOIUrl":"10.1016/j.semcancer.2025.06.006","url":null,"abstract":"<div><div>Obesity-associated insulin resistance (IR) is characterized by a chronic low-grade inflammatory state driven by adipocyte dysfunction, elevated free fatty acids, and proinflammatory cytokines. These factors activate signaling pathways—including JNK, TLR, and NF-κB—that impair insulin receptor function and promote hyperinsulinemia. Elevated insulin reduces insulin-like growth factor binding proteins, thereby increasing the bioavailability of IGF-1 and IGF-2, which stimulate oncogenic pathways such as PI3K-AKT-mTOR and RAS-MAPK. Epidemiological evidence links IR to an increased risk of a broad spectrum of malignancies, though associations vary by cancer subtype, patient demographics, and tumor characteristics. Therapeutic strategies targeting IR—ranging from lifestyle interventions and weight reduction to pharmacological agents like metformin and GLP-1 receptor agonists—have shown promise in reducing cancer risk and improving prognosis. Metformin exhibits anticancer effects through both AMPK-dependent and independent mechanisms, including mTOR inhibition, suppression of cell proliferation, and attenuation of oxidative stress. While observational studies support a relationship between improved insulin sensitivity and reduced cancer risk, definitive evidence from interventional trials remains limited. Overall, these findings underscore the critical role of metabolic dysfunction in tumorigenesis and highlight the potential of IR-targeted therapies in cancer prevention and management.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"114 ","pages":"Pages 73-87"},"PeriodicalIF":12.1,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Navigating the paradox of senescence and chemoresistance in pancreatic cancer 胰腺癌中衰老和化疗耐药的悖论。
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-06-11 DOI: 10.1016/j.semcancer.2025.06.007
Amal Jeiroshi , Juan Deng , Ziyao Xu , Annalisa Comandatore , Geng Xu , Antonino Glaviano , Luca Morelli , Ingrid Garajova , Elisa Giovannetti
Cellular senescence, described as a mechanism of irreversible cell cycle arrest, has emerged as a complex and multifaceted process with significant implications in cancer biology, particularly in pancreatic ductal adenocarcinoma (PDAC). This literature review aims to explore the intricate role of senescence in PDAC, focusing on its dual nature during tumorigenesis, in addition to therapy resistance, and its potential as a therapeutic target. Senescence escape was found to play a crucial role in PDAC progression, prompting the development of various pro-senescence therapies. However, recent studies have revealed a paradoxical aspect of the senescence-associated secretory phenotype, revealing its pro-tumorigenic effects and contribution to immune evasion in PDAC. By integrating insights from recent molecular studies, this review synthesizes current knowledge on the role of senescence in PDAC tumorigenesis and chemoresistance, with an emphasis on the emerging role of the tumor microenvironment and explores current and promising avenues for future research and potential therapeutic interventions.
细胞衰老被描述为一种不可逆的细胞周期停滞机制,是一个复杂的、多方面的过程,在癌症生物学中具有重要意义,特别是在胰腺导管腺癌(PDAC)中。本文献综述旨在探讨衰老在PDAC中的复杂作用,重点关注其在肿瘤发生过程中的双重性质,以及治疗耐药性,以及其作为治疗靶点的潜力。发现衰老逃逸在PDAC的进展中起着至关重要的作用,促进了各种促衰老疗法的发展。然而,最近的研究揭示了衰老相关分泌表型的一个矛盾方面,揭示了其在PDAC中的促肿瘤作用和免疫逃避作用。通过整合近期分子研究的见解,本文综合了衰老在PDAC肿瘤发生和化疗耐药中的作用的现有知识,重点介绍了肿瘤微环境的新作用,并探索了未来研究和潜在治疗干预的当前和有希望的途径。
{"title":"Navigating the paradox of senescence and chemoresistance in pancreatic cancer","authors":"Amal Jeiroshi ,&nbsp;Juan Deng ,&nbsp;Ziyao Xu ,&nbsp;Annalisa Comandatore ,&nbsp;Geng Xu ,&nbsp;Antonino Glaviano ,&nbsp;Luca Morelli ,&nbsp;Ingrid Garajova ,&nbsp;Elisa Giovannetti","doi":"10.1016/j.semcancer.2025.06.007","DOIUrl":"10.1016/j.semcancer.2025.06.007","url":null,"abstract":"<div><div>Cellular senescence, described as a mechanism of irreversible cell cycle arrest, has emerged as a complex and multifaceted process with significant implications in cancer biology, particularly in pancreatic ductal adenocarcinoma (PDAC). This literature review aims to explore the intricate role of senescence in PDAC, focusing on its dual nature during tumorigenesis, in addition to therapy resistance, and its potential as a therapeutic target. Senescence escape was found to play a crucial role in PDAC progression, prompting the development of various pro-senescence therapies. However, recent studies have revealed a paradoxical aspect of the senescence-associated secretory phenotype, revealing its pro-tumorigenic effects and contribution to immune evasion in PDAC. By integrating insights from recent molecular studies, this review synthesizes current knowledge on the role of senescence in PDAC tumorigenesis and chemoresistance, with an emphasis on the emerging role of the tumor microenvironment and explores current and promising avenues for future research and potential therapeutic interventions.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"114 ","pages":"Pages 60-72"},"PeriodicalIF":12.1,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The converging roles of microRNAs and lipid metabolism in atherosclerotic cardiovascular disease and cancer microrna和脂质代谢在动脉粥样硬化性心血管疾病和癌症中的聚合作用。
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-06-08 DOI: 10.1016/j.semcancer.2025.06.005
Sandra Vladimirov , Marija Tomasevic , Nemanja Popov , Jelena Munjas , David de Gonzalo-Calvo , Miron Sopic
Cancer and atherosclerotic cardiovascular disease (ASCVD) are the main causes of mortality worldwide. The complex relationship between these two diseases has long puzzled scientists, with lipid metabolism emerging as a promising area for research and therapy of both diseases. Cholesterol accumulation promotes the formation of atherosclerotic plaques, while dysregulated lipid metabolism favours the progression of tumours. MicroRNAs (miRNAs) have been identified as key post-transcriptional regulators of lipid metabolism, influencing cholesterol synthesis and efflux, fatty acid oxidation and lipoprotein function. MiR-33, miR-144 and miR-122 modulate important target proteins such as sterol regulatory element-binding proteins (SREBPs), ATP-binding cassette transporter A1 (ABCA1) and peroxisome proliferator-activated receptor gamma (PPARγ) and thus control metabolic reprogramming in both cancer and ASCVD. In cancer, miRNA-mediated lipid reprogramming promotes proliferation, immune evasion and metastasis, whereas dysregulated miRNAs in ASCVD contribute to foam cell formation, chronic inflammation and vascular dysfunction. The dual role of miRNAs, acting either as tumour suppressors or oncogenes, highlights their complex impact on lipid-related pathophysiology. Moreover, miRNA-based therapeutic strategies, including antagomirs and miRNA mimics, hold promise for targeted intervention in both diseases, which could reduce ASCVD risk in cancer patients and improve long-term outcomes. Understanding the intricate interactions between miRNAs, lipid metabolism and disease progression provides new insights into the overlapping molecular mechanisms of cancer and ASCVD and opens new therapeutic opportunities in the field of cardio-oncology.
癌症和动脉粥样硬化性心血管疾病(ASCVD)是世界范围内死亡的主要原因。长期以来,这两种疾病之间的复杂关系一直困扰着科学家,脂质代谢成为这两种疾病研究和治疗的一个有前景的领域。胆固醇积累促进动脉粥样硬化斑块的形成,而脂质代谢失调有利于肿瘤的进展。MicroRNAs (miRNAs)已被确定为脂质代谢的关键转录后调节因子,影响胆固醇的合成和外排、脂肪酸氧化和脂蛋白功能。MiR-33、miR-144和miR-122调节重要的靶蛋白,如甾醇调节元件结合蛋白(SREBPs)、atp结合盒转运蛋白A1 (ABCA1)和过氧化物酶体增殖激活受体γ (PPARγ),从而控制癌症和ASCVD的代谢重编程。在癌症中,mirna介导的脂质重编程促进增殖、免疫逃避和转移,而ASCVD中mirna失调有助于泡沫细胞形成、慢性炎症和血管功能障碍。mirna的双重作用,既可以作为肿瘤抑制因子,也可以作为致癌基因,突出了它们对脂质相关病理生理的复杂影响。此外,基于miRNA的治疗策略,包括安塔戈米和miRNA模拟物,有望对这两种疾病进行靶向干预,从而降低癌症患者的ASCVD风险并改善长期预后。了解mirna、脂质代谢和疾病进展之间复杂的相互作用,为癌症和ASCVD的重叠分子机制提供了新的见解,并为心脏肿瘤学领域开辟了新的治疗机会。
{"title":"The converging roles of microRNAs and lipid metabolism in atherosclerotic cardiovascular disease and cancer","authors":"Sandra Vladimirov ,&nbsp;Marija Tomasevic ,&nbsp;Nemanja Popov ,&nbsp;Jelena Munjas ,&nbsp;David de Gonzalo-Calvo ,&nbsp;Miron Sopic","doi":"10.1016/j.semcancer.2025.06.005","DOIUrl":"10.1016/j.semcancer.2025.06.005","url":null,"abstract":"<div><div>Cancer and atherosclerotic cardiovascular disease (ASCVD) are the main causes of mortality worldwide. The complex relationship between these two diseases has long puzzled scientists, with lipid metabolism emerging as a promising area for research and therapy of both diseases. Cholesterol accumulation promotes the formation of atherosclerotic plaques, while dysregulated lipid metabolism favours the progression of tumours. MicroRNAs (miRNAs) have been identified as key post-transcriptional regulators of lipid metabolism, influencing cholesterol synthesis and efflux, fatty acid oxidation and lipoprotein function. MiR-33, miR-144 and miR-122 modulate important target proteins such as sterol regulatory element-binding proteins (SREBPs), ATP-binding cassette transporter A1 (ABCA1) and peroxisome proliferator-activated receptor gamma (PPARγ) and thus control metabolic reprogramming in both cancer and ASCVD. In cancer, miRNA-mediated lipid reprogramming promotes proliferation, immune evasion and metastasis, whereas dysregulated miRNAs in ASCVD contribute to foam cell formation, chronic inflammation and vascular dysfunction. The dual role of miRNAs, acting either as tumour suppressors or oncogenes, highlights their complex impact on lipid-related pathophysiology. Moreover, miRNA-based therapeutic strategies, including antagomirs and miRNA mimics, hold promise for targeted intervention in both diseases, which could reduce ASCVD risk in cancer patients and improve long-term outcomes. Understanding the intricate interactions between miRNAs, lipid metabolism and disease progression provides new insights into the overlapping molecular mechanisms of cancer and ASCVD and opens new therapeutic opportunities in the field of cardio-oncology.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"114 ","pages":"Pages 41-59"},"PeriodicalIF":12.1,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144267235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Weighty matters: Unraveling the impact of obesity on colorectal cancer and nutritional interventions “重大问题:揭示肥胖对结直肠癌和营养干预的影响”。
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-06-06 DOI: 10.1016/j.semcancer.2025.06.004
Daniel Simancas-Racines , Claudia Reytor-González , Evelyn Frias-Toral , Christos S. Katsanos , Ricardo Hidalgo
This narrative review explores the influence of obesity on colorectal cancer, focusing on obesity-related factors, including chronic inflammation, metabolic dysregulation, and gut microbiota imbalance, which collectively create a pro-carcinogenic environment that increases colorectal cancer risk and complicates treatment outcomes. The findings indicate that obesity not only accelerates tumor progression but also presents challenges in colorectal cancer treatment, such as higher rates of surgical complications due to excess adipose tissue and altered pharmacokinetics that can reduce chemotherapy efficacy. Nutritional and lifestyle interventions, particularly weight management and anti-inflammatory nutritional therapies, are highlighted as effective strategies to reduce colorectal cancer risk and support treatment in patients with obesity. The study emphasizes the importance of personalized colorectal cancer treatment approaches for individuals with obesity and calls for public health policies targeting obesity prevention, which could significantly decrease colorectal cancer incidence and healthcare burdens associated with this high-risk population.
本综述探讨了肥胖对结直肠癌的影响,重点关注肥胖相关因素,包括慢性炎症、代谢失调和肠道微生物群失衡,这些因素共同创造了一个致癌环境,增加了结直肠癌的风险并使治疗结果复杂化。研究结果表明,肥胖不仅加速了肿瘤的进展,而且给结直肠癌的治疗带来了挑战,例如由于脂肪组织过多和药物代谢动力学改变而导致的手术并发症发生率更高,从而降低了化疗效果。营养和生活方式干预,特别是体重管理和抗炎营养疗法,被强调为降低结直肠癌风险和支持肥胖患者治疗的有效策略。该研究强调了个性化结直肠癌治疗方法对肥胖个体的重要性,并呼吁制定针对肥胖预防的公共卫生政策,这可能会显著降低结直肠癌发病率和与这一高危人群相关的医疗负担。
{"title":"Weighty matters: Unraveling the impact of obesity on colorectal cancer and nutritional interventions","authors":"Daniel Simancas-Racines ,&nbsp;Claudia Reytor-González ,&nbsp;Evelyn Frias-Toral ,&nbsp;Christos S. Katsanos ,&nbsp;Ricardo Hidalgo","doi":"10.1016/j.semcancer.2025.06.004","DOIUrl":"10.1016/j.semcancer.2025.06.004","url":null,"abstract":"<div><div>This narrative review explores the influence of obesity on colorectal cancer, focusing on obesity-related factors, including chronic inflammation, metabolic dysregulation, and gut microbiota imbalance, which collectively create a pro-carcinogenic environment that increases colorectal cancer risk and complicates treatment outcomes. The findings indicate that obesity not only accelerates tumor progression but also presents challenges in colorectal cancer treatment, such as higher rates of surgical complications due to excess adipose tissue and altered pharmacokinetics that can reduce chemotherapy efficacy. Nutritional and lifestyle interventions, particularly weight management and anti-inflammatory nutritional therapies, are highlighted as effective strategies to reduce colorectal cancer risk and support treatment in patients with obesity. The study emphasizes the importance of personalized colorectal cancer treatment approaches for individuals with obesity and calls for public health policies targeting obesity prevention, which could significantly decrease colorectal cancer incidence and healthcare burdens associated with this high-risk population.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"114 ","pages":"Pages 29-40"},"PeriodicalIF":12.1,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
"Time" for obesity-related cancers: The role of chrononutrition in cancer prevention and treatment 肥胖相关癌症的“时间”:时间营养在癌症预防和治疗中的作用
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-06-03 DOI: 10.1016/j.semcancer.2025.06.002
Ludovica Verde , Martina Galasso , Silvia Savastano , Annamaria Colao , Luigi Barrea , Giovanna Muscogiuri
Obesity-related cancers are increasing globally, driven by metabolic disturbances and circadian rhythm disruptions. Circadian rhythms regulate physiological processes, and their misalignment has been linked to increased cancer risk. Chrononutrition, which aligns dietary intake with the body's circadian clock, has emerged as a potential strategy for cancer prevention and treatment. This review explored the intricate relationship between circadian rhythm, metabolism, and cancer, highlighting the role of meal timing, macronutrient distribution, fasting, and ketogenic diets. Additionally, the potential synergy between chrononutrition and cancer therapies was discussed, emphasizing the need for personalized approaches. Future research should focus on integrating chrononutritional strategies into clinical practice to enhance treatment outcomes and improve quality of life in patients with obesity-related cancers.
由于代谢紊乱和昼夜节律紊乱,与肥胖相关的癌症在全球范围内正在增加。昼夜节律调节着生理过程,它们的失调与癌症风险的增加有关。时间营养使饮食摄入与人体生物钟保持一致,已成为预防和治疗癌症的潜在策略。这篇综述探讨了昼夜节律、代谢和癌症之间的复杂关系,强调了进餐时间、宏量营养素分布、禁食和生酮饮食的作用。此外,还讨论了时间营养与癌症治疗之间的潜在协同作用,强调了个性化治疗方法的必要性。未来的研究应侧重于将时间营养策略整合到临床实践中,以提高肥胖相关癌症患者的治疗效果和生活质量。
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引用次数: 0
Long-term recurrence of PDAC after resection for IPMN: A narrative review of the literature on clinical and biologic predictors IPMN切除后PDAC的长期复发:临床和生物学预测文献的叙述性回顾
IF 12.1 1区 医学 Q1 ONCOLOGY Pub Date : 2025-06-02 DOI: 10.1016/j.semcancer.2025.06.001
Annalisa Comandatore , Gregorio Di Franco , Ingrid Garajová , Afrodita Panaitescu , Fabio Ausania , Livia Giannessi , Niccoló Furbetta , Simone Guadagni , Anna Caterina Milanetto , Claudio Pasquali , Manuel Gentiluomo , Chiara Corradi , Volkan Adsay , Daniele Campa , Elisa Giovannetti , Luca Morelli
Recurrence of IPMNs after surgical resection is defined as the reappearance of new cystic lesions, invasive carcinoma, or metastases, either in the remnant pancreas or other distant sites. The median 5-year cumulative incidence of residual pancreatic lesions is 10 % (range, 0–21 %) and this risk continues to increase even after five years, especially in patients with the presence of HGD at first surgery and a family history of pancreatic ductal adenocarcinoma (PDAC). The management algorithm for all IPMNs is described in the latest guidelines on IPMNs; the patient's general condition, comorbidities, and life expectancy should be considered as well in the surgical decision. All patients operated for IPMN, have a risk of developing metachronous pancreatic lesions, which may require further surgery. Therefore, postoperative surveillance should be continued until the patient is surgically fit. The primary objective of this review is to evaluate the current scientific evidence regarding the management and surveillance strategies in patients who have undergone surgery for IPMN. Secondarily, we assessed the definitions of recurrence after surgery and explored the clinical, pathological, and biomolecular factors which may influence the biologic behavior of IPMNs. The optimal surveillance strategy for resected IPMN remains a topic of ongoing debate. The presence of an enlarging mass, the increase of ductal diameter, extrapancreatic disease observed during postoperative CT scans were previously taken into account as possible recurrence indicators. Additionally, positive resection margins, tumor invasiveness, and lymph node involvement were previously correlated with recurrence, while the role of molecular biomarkers still needs to bevalidated. This underscores the importance of rigorous, long-term follow-up, with multimodal approach as recurrent IPMNs can be detected even more than five years post-surgery.
手术切除后IPMNs的复发定义为在残余胰腺或其他远处部位出现新的囊性病变、浸润性癌或转移。胰腺残余病变5年累积发生率中位数为10 %(范围0-21 %),即使在5年后,这种风险仍在继续增加,特别是在首次手术时存在HGD和有胰腺导管腺癌(PDAC)家族史的患者。最新的IPMNs指南描述了所有IPMNs的管理算法;患者的一般情况,合并症和预期寿命也应考虑到手术的决定。所有因IPMN手术的患者都有发生异时性胰腺病变的风险,这可能需要进一步的手术。因此,术后监测应继续进行,直到患者适合手术。本综述的主要目的是评估目前关于IPMN手术患者的管理和监测策略的科学证据。其次,我们评估了术后复发的定义,并探讨了可能影响IPMNs生物学行为的临床、病理和生物分子因素。对于切除的IPMN的最佳监测策略仍然是一个持续争论的话题。术后CT扫描中观察到肿物增大、导管直径增大、胰腺外病变等,以前被认为是可能的复发指标。此外,阳性切除边缘、肿瘤侵袭性和淋巴结累及先前与复发相关,而分子生物标志物的作用仍需要验证。这强调了严格、长期随访和多模式方法的重要性,因为复发性IPMNs甚至可以在手术后5年以上被发现。
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Seminars in cancer biology
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