Seminars in oncology最新文献_第3页

Artificial intelligence-driven intelligent nanocarriers for cancer theranostics: A paradigm shift with focus on brain tumors 用于癌症治疗的人工智能驱动的智能纳米载体：以脑肿瘤为重点的范式转变。

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-12-01 Epub Date: 2025-11-10 DOI: 10.1016/j.seminoncol.2025.152429

Mehrab Pourmadadi , Salar Mohammadi Shabestari , Hamidreza Abdouss , Abbas Rahdar , Sonia Fathi-Karkan , Sadanand Pandey

Artificial intelligence (AI) and nanotechnology are revolutionizing brain cancer theranostics by enhancing drug delivery and diagnostic accuracy. This review examines AI-enhanced engineering strategies for developing intelligent nanocarriers that target glioblastoma and other metastatic central nervous system malignancies. AI encompasses several computational methods, including machine learning (ML) and its subset deep learning (DL). Here, ML algorithms learn design rules for nanocarriers, and DL networks intricate pattern recognition for tumor segmentation and adaptive release. These approaches enable stimuli-responsive nanocarriers to react to tumor microenvironmental signals (eg, pH, enzyme activity) and external stimuli (eg, ultrasound), optimizing targeted medication release while minimizing off-target effects. Magnetic resonance imaging (MRI) and positron emission tomography (PET), in conjunction with AI, enhance tumor detection and segmentation, while the integration of multiomics data facilitates tailored treatment planning. Advanced technologies encompass transferrin-functionalized nanoparticles for traversing the blood-brain barrier (BBB) and dual-stimuli-responsive drug delivery systems. Notwithstanding general progress, apprehensions surrounding batch variability and industrial scalability persist. This review also addresses ethical concerns and cost disparities associated with AI-based therapeutics. The primary development target areas are federated learning for data privacy, explainable artificial intelligence (XAI) for regulatory transparency, and quantum ML for molecular-scale optimization. This paper charts the course to patient-specific, scalable neuro-oncology nanomedicine through the convergence of computational modeling, intelligent materials, and advanced imaging modalities. These themes are explored in greater detail in the introduction, where we lay the groundwork for intelligent nanocarriers, their design with the help of AI, and the clinical need for diagnostics-therapeutics convergence in brain cancer.

人工智能（AI）和纳米技术通过增强药物传递和诊断准确性，正在彻底改变脑癌治疗方法。本文综述了人工智能增强的工程策略，用于开发针对胶质母细胞瘤和其他转移性中枢神经系统恶性肿瘤的智能纳米载体。人工智能包括几种计算方法，包括机器学习（ML）及其子集深度学习（DL）。在这里，机器学习算法学习纳米载体的设计规则，深度学习网络复杂的模式识别用于肿瘤分割和自适应释放。这些方法使刺激反应性纳米载体能够对肿瘤微环境信号（如pH值、酶活性）和外部刺激（如超声）做出反应，优化靶向药物释放，同时最大限度地减少脱靶效应。磁共振成像（MRI）和正电子发射断层扫描（PET）与人工智能相结合，增强了肿瘤的检测和分割，而多组学数据的整合有助于制定量身定制的治疗计划。先进的技术包括用于穿越血脑屏障（BBB）的转铁蛋白功能化纳米颗粒和双刺激反应性药物递送系统。尽管总体上取得了进展，但对批处理可变性和工业可扩展性的担忧仍然存在。本综述还讨论了与人工智能治疗相关的伦理问题和成本差异。主要的发展目标领域是用于数据隐私的联邦学习、用于监管透明度的可解释人工智能（XAI）和用于分子尺度优化的量子机器学习。本文通过计算建模、智能材料和先进成像方式的融合，描绘了患者特异性、可扩展的神经肿瘤纳米医学的过程。这些主题在引言中进行了更详细的探讨，我们为智能纳米载体、它们在人工智能的帮助下的设计以及脑癌诊断治疗融合的临床需求奠定了基础。

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引用次数: 0

Mapping the epidemiology of cancer-related anemia: A systematic scoping review of global prevalence and incidence 绘制癌症相关性贫血的流行病学：全球患病率和发病率的系统范围审查。

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-12-01 Epub Date: 2025-10-04 DOI: 10.1016/j.seminoncol.2025.152426

Dana Elkhalifa BSc, MSc , Marjolijn N Lub-de Hooge PharmD, PhD , Frank GA Jansman PharmD, PhD

Cancer-related anemia (CRA) is a common and debilitating condition among oncology patients, driven by tumor burden, treatment toxicity, nutritional deficiencies, and systemic inflammation. This review aims to synthesize evidence on the global and geographical prevalence and incidence patterns of CRA. A systematic search of PubMed and Embase identified English-language studies on CRA published was performed between 2000 and November 30, 2024. Observational studies and clinical trials reporting CRA prevalence and/or incidence were included. Extracted data covered country, study design, patient demographics, cancer type, anemia classification, and CRA incidence/prevalence rates. The data were then charted by geographical locations. A total of 42 studies, encompassing 65,179 cancer patients across 5 continents and 40 countries, were included. CRA prevalence ranged from 12.8% to 100%, with the highest rates reported in lung (84.2%), pediatric cancers (80.9%), gynecological (62.99%), and gastrointestinal (57.4%) cancers. The composite prevalence of anemia across multiple cancer types and solid tumors was 64.99% and 25.68%, respectively. However, cancer-type-specific analyses often reported higher prevalence rates than composite outcomes, with variations largely influenced by geographical location. Chemotherapy and radiotherapy were consistently associated with increased incidence, with post-treatment anemia prevalence reaching 100% in some cohorts. Regional disparities were noted, particularly in Africa, South America, and the Middle East and North Africa (MENA) region. CRA is a globally prevalent condition, with rates influenced by cancer type, geographic region, and the initiation of chemotherapy or radiotherapy. Future research should prioritize standardized reporting and address regional data gaps.

肿瘤相关性贫血（CRA）是肿瘤患者中一种常见的衰弱性疾病，由肿瘤负担、治疗毒性、营养缺乏和全身性炎症驱动。这篇综述的目的是综合证据的全球和地理流行和发病率模式的CRA。对PubMed和Embase进行了系统搜索，确定了2000年至2024年11月30日期间发表的关于CRA的英语研究。报告CRA患病率和/或发病率的观察性研究和临床试验被纳入。提取的数据涵盖国家、研究设计、患者人口统计、癌症类型、贫血分类和CRA发病率/患病率。然后将数据按地理位置绘制成图表。共纳入了42项研究，涉及5大洲40个国家的65179名癌症患者。CRA患病率从12.8%到100%不等，其中肺癌（84.2%）、儿科癌症（80.9%）、妇科癌症（62.99%）和胃肠道癌症（57.4%）的发病率最高。多种癌症类型和实体肿瘤的贫血综合患病率分别为64.99%和25.68%。然而，癌症类型特异性分析通常报告的患病率高于综合结果，其差异在很大程度上受地理位置的影响。化疗和放疗始终与发病率增加相关，在一些队列中，治疗后贫血患病率达到100%。注意到区域差异，特别是在非洲、南美洲、中东和北非区域。CRA是一种全球流行的疾病，其发病率受癌症类型、地理区域和化疗或放疗开始的影响。未来的研究应优先考虑标准化报告和解决区域数据差距。

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引用次数: 0

Sex-differential responses to immune checkpoint inhibitors across the disease continuum unified by tumor mutational burden 通过肿瘤突变负担统一的疾病连续体中免疫检查点抑制剂的性别差异反应

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-12-01 Epub Date: 2025-09-03 DOI: 10.1016/j.seminoncol.2025.152414

Ming Zheng MD, PhD

While the efficacy of immune checkpoint inhibitors (ICIs) in advanced non–small-cell lung cancer (NSCLC) is well-established, sex-based differences in treatment responses remain insufficiently explored. This study examines how sex disparities impact ICI treatment outcomes in advanced-stage NSCLC, focusing on the role of tumor mutational burden (TMB) in these differences. This study analyzed data from 174 advanced-stage, chemotherapy-naïve, NSCLC patients treated with ICIs, including PD-1/PD-L1 and CTLA-4 inhibitors, to assess sex differences in treatment response and survival outcomes. Male patients with low TMB (<10 mut/Mb) had worse treatment responses compared to female patients. In contrast, no sex differences were observed in patients with high TMB, where both sexes exhibited similar therapeutic responses. These results suggest that high TMB may reduce the impact of sex on ICI efficacy, with male and female patients showing comparable outcomes. Furthermore, sex disparities in disease progression and overall survival were more evident in low-TMB patients, emphasizing the role of TMB in modulating sex-related differences in immunotherapy outcomes. This study highlights the importance of incorporating both sex and TMB into precision oncology. High TMB appears to equalize treatment responses between sexes, while low TMB may necessitate more personalized treatment strategies, particularly for male patients. Further research into the biological mechanisms underlying these differences is essential to optimize ICI therapies and enhance patient outcomes. Integrating both sex and TMB into clinical decision-making will help to develop more tailored and effective cancer immunotherapy.

虽然免疫检查点抑制剂（ICIs）在晚期非小细胞肺癌（NSCLC）中的疗效已得到证实，但基于性别的治疗反应差异仍未得到充分探讨。本研究探讨了性别差异如何影响晚期NSCLC的ICI治疗结果，重点关注肿瘤突变负担（tumor mutational burden， TMB）在这些差异中的作用。本研究分析了174例晚期（chemotherapy-naïve） NSCLC患者接受ICIs治疗的数据，包括PD-1/PD-L1和CTLA-4抑制剂，以评估治疗反应和生存结果的性别差异。低TMB （<10 mut/Mb）的男性患者治疗反应较女性患者差。相比之下，在高TMB患者中没有观察到性别差异，其中两性表现出相似的治疗反应。这些结果表明，高TMB可能会降低性别对ICI疗效的影响，男性和女性患者的结果相当。此外，在低TMB患者中，疾病进展和总生存期的性别差异更为明显，强调了TMB在调节免疫治疗结果的性别相关差异中的作用。这项研究强调了将性别和TMB纳入精确肿瘤学的重要性。高TMB似乎使两性之间的治疗反应相等，而低TMB可能需要更个性化的治疗策略，特别是对于男性患者。进一步研究这些差异背后的生物学机制对于优化ICI治疗和提高患者预后至关重要。将性别和TMB纳入临床决策将有助于开发更有针对性和更有效的癌症免疫疗法。

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引用次数: 0

Purine metabolism in tumorigenesis and its clinical implications 嘌呤代谢在肿瘤发生中的作用及其临床意义

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-12-01 Epub Date: 2025-09-02 DOI: 10.1016/j.seminoncol.2025.152409

Zerui Lu , Jiayi Li , Ying Liu , Hui Li , Ying Sun , Rui Geng , Jiahang Song , Jinhui Liu

Metabolic reprogramming constitutes a hallmark of malignant neoplasms. Purine metabolism emerges as a pivotal regulator in cellular metabolic networks through multiple mechanisms, including dysregulation of de novo biosynthesis/salvage pathway coordination, adenosine-mediated immunosuppressive microenvironment formation, and collective contributions to tumorigenesis and malignant progression. During metastatic progression, purine metabolism reinforces tumor cell plasticity through mitochondrial energy regulation and modulation of cell cycle checkpoints (eg, G1/S transition). These mechanistic revelations have positioned purine metabolism-targeting strategies as promising oncotherapeutic candidates. This review methodically analyzes (1) purine metabolic pathways and their regulatory dynamics, (2) adenosine-mediated pathophysiological interactions, and (3) the synergistic impacts of these pathways in malignant transformation. We propose a unified mechanistic framework that clarifies oncogenic purine metabolic rewiring while evaluating translational potential through three clinical dimensions: pathogenesis elucidation, diagnostic biomarker discovery, and targeted therapeutic development. This comprehensive synthesis aims to advance precision oncology through mechanistic insights and therapeutic innovation.

代谢重编程是恶性肿瘤的一个特征。嘌呤代谢通过多种机制在细胞代谢网络中发挥关键调节作用，包括对新生生物合成/挽救途径协调的失调、腺苷介导的免疫抑制微环境的形成以及对肿瘤发生和恶性进展的共同贡献。在转移过程中，嘌呤代谢通过线粒体能量调节和细胞周期检查点（如G1/S转变）的调节来增强肿瘤细胞的可塑性。这些机制的揭示已经定位嘌呤代谢靶向策略作为有希望的肿瘤治疗候选人。本文系统分析了(1)嘌呤代谢途径及其调控动力学，(2)腺苷介导的病理生理相互作用，以及(3)这些途径在恶性转化中的协同作用。我们提出了一个统一的机制框架来阐明致癌嘌呤代谢重布线，同时通过三个临床维度评估转化潜力：发病机制阐明、诊断性生物标志物发现和靶向治疗开发。这一全面的综合旨在通过机制见解和治疗创新来推进精准肿瘤学。

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引用次数: 0

Unveiling the role of RAI14 in cancer: Biological significance and translational perspectives 揭示RAI14在癌症中的作用：生物学意义和翻译观点

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-12-01 Epub Date: 2025-09-02 DOI: 10.1016/j.seminoncol.2025.152412

Zhi-Xiong Chong

Retinoic acid-induced protein 14 (RAI14) is an actin-binding protein that regulates actin dynamics, cell adhesion, and migration. RAI14 dysregulation has been reported to facilitate the development of at least 10 tumor types based on the findings from over 20 original research articles. This review article aims to fill in the gap in the literature by providing a comprehensive summary of the putative tumor-regulatory roles of RAI14 in different cancers. Overall, RAI14 can affect protein kinase B (AKT), mammalian target of rapamycin, yes-associated protein/Hippo, apoptosis, and epithelial-to-mesenchymal transition activities to promote tumorigenesis. Several noncoding RNAs like miR-23b-3p and AFAP1-AS1 can directly or indirectly affect RAI14 expression to control its tumor-modulatory function epigenetically. Additionally, RAI14 tissue or serum level are overexpressed in at least seven human tumors, including breast, gastrointestinal, genitourinary, and brain cancers. This gives RAI14 the translational potential as a diagnostic or prognostic biomarker. Targeting RAI14 as a cancer antigen can also potentially help halt tumor progression. Future large-scale trials are needed to confirm the tumor-regulatory role of RAI14 in human cancer and to evaluate the sensitivity, reliability, and accuracy of using this target as a biomarker or therapeutic target.

视黄酸诱导蛋白14 （Retinoic acid-induced protein 14, RAI14）是一种肌动蛋白结合蛋白，可调节肌动蛋白动力学、细胞粘附和迁移。根据20多篇原创研究文章的发现，RAI14失调已被报道促进了至少10种肿瘤类型的发展。本文旨在通过全面总结RAI14在不同癌症中可能的肿瘤调节作用来填补这一文献空白。总体而言，RAI14可以影响蛋白激酶B （AKT）、哺乳动物雷帕霉素靶点、酵母相关蛋白/Hippo、细胞凋亡和上皮间质转化活性，从而促进肿瘤发生。miR-23b-3p、AFAP1-AS1等几种非编码rna可直接或间接影响RAI14的表达，从表观遗传上控制其肿瘤调节功能。此外，RAI14在至少7种人类肿瘤中组织或血清水平过表达，包括乳腺癌、胃肠道、泌尿生殖系统和脑癌。这使得RAI14具有作为诊断或预后生物标志物的翻译潜力。靶向RAI14作为癌症抗原也可能有助于阻止肿瘤进展。未来的大规模试验需要证实RAI14在人类癌症中的肿瘤调节作用，并评估使用该靶点作为生物标志物或治疗靶点的敏感性、可靠性和准确性。

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引用次数: 0

Corrigendum to “Epidemiology and prevention of gastric cancer: A comprehensive review” [Seminars in Oncology Volume 52 (2025) 152341] “流行病学和预防胃癌：全面审查”[肿瘤学研讨会卷52(2025)152341]的勘误表。

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-12-01 Epub Date: 2025-09-30 DOI: 10.1016/j.seminoncol.2025.152424

Smruti Priyambada Pradhan , Ayushman Gadnayak , Sukanta Kumar Pradhan , Venkatarao Epari

引用次数: 0

Pretreatment eosinophilia as a biomarker for adverse outcomes in non-small cell lung cancer patients receiving immune checkpoint inhibitors: A systematic review and meta-analysis 预处理嗜酸性粒细胞增多作为接受免疫检查点抑制剂的非小细胞肺癌患者不良结局的生物标志物：一项系统综述和荟萃分析

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-12-01 Epub Date: 2025-11-03 DOI: 10.1016/j.seminoncol.2025.152431

Nency Ganatra , Jacob Thompson , Rupak Desai , Jinish Doshi , Pragya Jain , Diksha Sanjana Pasnoor , Akhil Jain

In recent years, immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of non-small cell lung cancer (NSCLC), yet treatment response and adverse events vary widely among patients. In response, the identification of reliable pretreatment biomarkers has become a major goal for many clinicians to enhance prognostication and personalized care. As such, this systematic review and meta-analysis aimed to evaluate whether pretreatment eosinophilia is associated with adverse clinical outcomes in NSCLC patients receiving ICI therapy. Following PRISMA guidelines, a comprehensive literature search was conducted across online databases through February 2025. Eligible studies included observational designs reporting associations between baseline eosinophil levels and overall survival, progression-free survival, or immune-related adverse events (irAEs) in ICI-treated NSCLC patients. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using random-effects models for both unadjusted and adjusted data. Eleven studies met inclusion criteria. Pretreatment eosinophilia was associated with a nonsignificant reduction in overall survival based on both unadjusted analyses (OR: 0.79, 95% CI: 0.42–1.51 and OR: 0.74, 95% CI: 0.53–1.03, respectively). Similarly, a nonsignificant reduction in progression-free survival was found in unadjusted models (OR: 0.78, 95% CI: 0.54–1.13), whereas adjusted data revealed a significant negative association (OR: 0.68, 95% CI: 0.58–0.80). In contrast, eosinophilia was significantly associated with increased odds of irAEs in both unadjusted and adjusted analyses (OR: 3.19, 95% CI: 2.11–4.83 and OR: 3.35, 95% CI: 2.25–5.02, respectively). These findings indicate that pretreatment eosinophilia may serve as a useful prognostic biomarker indicating increased susceptibility to irAEs and potentially poorer survival outcomes in ICI-treated NSCLC patients.

近年来，免疫检查点抑制剂（ICIs）已经改变了非小细胞肺癌（NSCLC）的治疗前景，但不同患者的治疗反应和不良事件差异很大。因此，确定可靠的预处理生物标志物已成为许多临床医生提高预后和个性化护理的主要目标。因此，本系统综述和荟萃分析旨在评估在接受ICI治疗的非小细胞肺癌患者中，预处理嗜酸性粒细胞增多是否与不良临床结果相关。按照PRISMA的指导方针，在2025年2月之前对在线数据库进行了全面的文献检索。符合条件的研究包括观察性设计，报告基线嗜酸性粒细胞水平与ici治疗的非小细胞肺癌患者的总生存期、无进展生存期或免疫相关不良事件（irAEs）之间的关联。使用随机效应模型计算未调整和调整数据的合并优势比（ORs）和95%置信区间（ci）。11项研究符合纳入标准。未经调整的两项分析显示，预处理嗜酸性粒细胞增多与总生存期无显著降低相关（OR分别为0.79,95% CI: 0.42-1.51和OR: 0.74, 95% CI: 0.53-1.03）。同样，在未调整的模型中发现无进展生存期无显著降低（OR: 0.78, 95% CI: 0.54-1.13），而调整后的数据显示显著负相关（OR: 0.68, 95% CI: 0.58-0.80）。相比之下，在未调整和调整的分析中，嗜酸性粒细胞增多与irae的发生率增加显著相关（OR: 3.19, 95% CI: 2.11-4.83; OR: 3.35, 95% CI: 2.25-5.02）。这些发现表明，预处理嗜酸性粒细胞增多可能是一种有用的预后生物标志物，表明ici治疗的非小细胞肺癌患者对irae的易感性增加，生存结果可能更差。

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引用次数: 0

The effects of microbiota-derived short-chain fatty acids on T lymphocytes: From autoimmune diseases to cancer 微生物源性短链脂肪酸对T淋巴细胞的影响：从自身免疫性疾病到癌症

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-10-01 Epub Date: 2025-08-19 DOI: 10.1016/j.seminoncol.2025.152398

Mohamed J. Saadh , Omer Qutaiba B. Allela , Suhas Ballal , Morug Salih Mahdi , Mamata Chahar , Rajni Verma , Rouaida Kadhim A Al-hussein , Mohaned Adil , Mahmood Jasem Jawad , Ali M. Ali Al-Nuaimi

Short-chain fatty acids (SCFAs), acetate, propionate, and butyrate, are the microbial metabolites that have significant functions in host immune modulation, especially T lymphocyte function. Implication by recent evidence indicates SCFAs regulate T-cell growth, differentiation, metabolism, effector function, and apoptosis through histone deacetylase (HDAC) inhibition, G-protein-coupled receptor (GPCR) signaling, and metabolic reprogramming processes. Butyrate, for example, enhances regulatory T cell (Treg) and Interleukin 10 (IL-10)-producing T helper 1 (Th1) cell differentiation as well as context-dependent regulation on T helper 17 (Th17) cell development. SCFAs also impact cytotoxic CD8+ T cells through augmented production of IFN-γ and memory formation, which enhances antiviral and antitumor immunity. SCFAs reprogram T-cell metabolism through enhanced acetyl-CoA, mechanistic target of rapamycin (mTOR) signaling, and fatty acid oxidation (FAO), thus promoting the unique metabolic requirements of effector and memory T-cell subsets. In addition, SCFAs induce apoptosis of activated T cells through the Fas upregulation by inhibiting HDAC1. SCFA dysregulation plays a role in disease and autoimmune disorders like type 1 diabetes and rheumatoid arthritis, whereas therapeutic supplementation reduces inflammation and immune tolerance. SCFAs also amplify the antitumor effect of immune checkpoint inhibitors (eg, anti-programmed cell death protein 1 (anti-PD-1)) in cancer by driving CD8+ T-cell activation, infiltration, and Interferon gamma (IFNγ) production, partially through the transcriptional regulator Inhibitor of DNA binding 2 (ID2). Significantly, tissue- and disease-specific differential expression and functional implication of SCFA receptors (eg, GPR43, GPR41, GPR109A) emphasize the complexity of SCFA-mediated signaling. In conclusion, the current review emphasizes the multifunctional role of microbiota-derived SCFAs in T lymphocyte biology and their therapeutic potential in cancer, infection, and autoimmune diseases.

短链脂肪酸（SCFAs），醋酸酯、丙酸酯和丁酸酯是在宿主免疫调节，特别是T淋巴细胞功能中具有重要功能的微生物代谢物。最近的证据表明，SCFAs通过抑制组蛋白去乙酰化酶（HDAC）、g蛋白偶联受体（GPCR）信号传导和代谢重编程过程调节t细胞的生长、分化、代谢、效应功能和凋亡。例如，丁酸盐可以增强调节性T细胞（Treg）和产生白细胞介素10 （IL-10）的辅助性T细胞1 （Th1）细胞的分化，以及对辅助性T细胞17 （Th17）细胞发育的环境依赖性调节。SCFAs还通过增加IFN-γ的产生和记忆形成来影响细胞毒性CD8+ T细胞，从而增强抗病毒和抗肿瘤免疫。SCFAs通过增强乙酰辅酶a、雷帕霉素（mTOR）信号传导机制靶点和脂肪酸氧化（FAO）来重编程t细胞代谢，从而促进效应t细胞亚群和记忆t细胞亚群独特的代谢需求。此外，SCFAs通过抑制HDAC1而上调Fas，诱导活化的T细胞凋亡。SCFA失调在1型糖尿病和类风湿性关节炎等疾病和自身免疫性疾病中发挥作用，而治疗性补充可减少炎症和免疫耐受。SCFAs还通过驱动CD8+ t细胞活化、浸润和干扰素γ (IFNγ)的产生，部分通过转录调节因子DNA结合2抑制剂（ID2），增强了免疫检查点抑制剂（例如抗程序性细胞死亡蛋白1 (anti-PD-1)）在癌症中的抗肿瘤作用。值得注意的是，组织和疾病特异性的SCFA受体（如GPR43、GPR41、GPR109A）的差异表达和功能意义强调了SCFA介导的信号传导的复杂性。总之，本综述强调了微生物来源的SCFAs在T淋巴细胞生物学中的多功能作用及其在癌症、感染和自身免疫性疾病中的治疗潜力。

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引用次数: 0

Overexpression of CAD in stomach adenocarcinoma tissues and its clinical significance CAD在胃腺癌组织中的过表达及其临床意义

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-10-01 Epub Date: 2025-08-11 DOI: 10.1016/j.seminoncol.2025.152396

Siyi Wang , Hang Xing , Meiting Long , Min Zhou , Zhe Wang , Bingchen Hou , Steven Mo , Di Na , Shanshan Bu

Stomach adenocarcinoma (STAD) is one of the deadliest malignant tumors worldwide. Carbamoyl-phosphate synthetase 2 (CAD) expression is essential for categorizing and detecting STAD initiation and development. We explored the differential expression of genes (DEGs) affected by CAD overexpression and subsequently revealed the classification module of CAD-based scoring sets using weighted gene co-expression network analysis (WGCNA). Subsequently, enrichment analysis of biological functions and signaling pathways in clinically significant modules was conducted. We constructed a CAD-based clinical scoring model using univariate and multivariate Cox regression analyses. In addition, by using immune cell infiltration analysis, we investigated the interaction between CAD-based score and the immune microenvironment, identified upstream regulatory factors, including RNA binding proteins (RBPs), that affect the transcription of the STAD-related CAD-based score, and explored potential drug targets. We identified 4,977 abnormal regulatory genes related to CAD in STAD, among which the module genes most related to CAD were significantly enriched in cancer-related signaling pathways, such as VEGF, MAPK and TGF-beta signaling pathway. The CAD-based scores, T and N were identified as independent prognostic factors for STAD patients. We also found that under the influence of high expression of CAD, the infiltration level of most immune cells is lower, such as CD4 T cells and Tfh, and CAD has an inhibitory effect on the infiltration of certain immune cells. Notably, the potential drug targets PDHB and NDUFB6 are upstream regulatory factors in STAD. This study explored the role of highly expressed CAD-related genes in STAD and explored the tumorigenesis and progression of this disease. This research identified potential diagnostic and prognostic drug targets and provided new insights into the molecular mechanisms of STAD.

胃腺癌（STAD）是世界上最致命的恶性肿瘤之一。氨甲酰磷酸合成酶2 （CAD）的表达对于STAD的发生和发展的分类和检测至关重要。我们探索了受CAD过表达影响的基因（deg）的差异表达，随后使用加权基因共表达网络分析（WGCNA）揭示了基于CAD的评分集的分类模块。随后，对临床重要模块的生物学功能和信号通路进行富集分析。我们使用单变量和多变量Cox回归分析构建了基于cad的临床评分模型。此外，通过免疫细胞浸润分析，我们研究了基于cad的评分与免疫微环境之间的相互作用，确定了上游调控因子，包括RNA结合蛋白（rbp），影响stad相关的基于cad的评分的转录，并探索了潜在的药物靶点。我们在STAD中发现了4977个与CAD相关的异常调控基因，其中与CAD最相关的模块基因在肿瘤相关信号通路中显著富集，如VEGF、MAPK和tgf - β信号通路。基于cad的评分、T和N被确定为STAD患者的独立预后因素。我们还发现，在CAD高表达的影响下，大多数免疫细胞的浸润水平降低，如CD4 T细胞和Tfh， CAD对某些免疫细胞的浸润有抑制作用。值得注意的是，潜在的药物靶点PDHB和NDUFB6是STAD的上游调控因子。本研究探讨了高表达的cad相关基因在STAD中的作用，并探讨了该疾病的肿瘤发生和进展。本研究确定了潜在的诊断和预后药物靶点，并为STAD的分子机制提供了新的见解。

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引用次数: 0

Prostate cancer in Türkiye: Trend analysis of incidence and mortality rates 日本前列腺癌：发病率和死亡率的趋势分析

IF 3 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-10-01 Epub Date: 2025-07-19 DOI: 10.1016/j.seminoncol.2025.152391

Guven Turan , Merve Turan , Yasemin Basbinar , Hulya Ellidokuz

Prostate cancer is a significant global health concern, with substantial regional variations in incidence and mortality rates. In Türkiye, it's the second most common cancer and fourth leading cause of cancer-related deaths among men. This study aims to analyze trends in prostate cancer incidence and mortality rates in Türkiye. Prostate cancer trends in Türkiye is analyzed by using data of incidence from Türkiye Cancer Statistics Reports and mortality from TurkStat. Trends in incidence and mortality rates were analyzed using Joinpoint regression, evaluating average annual percentage changes and annual percentage change (APC). From 2004 to 2018, age-standardized prostate cancer incidence rate increased from 24.9 to 40.3 per 100,000, with the highest in aged 75 and older. The Annual Average Percentage Change (AAPC) was 2.6%[CI, 1.1 to 4.3] overall, with specific rates of 2.3% [CI, 0.5 to 3.5] in the 50–54 and −1.9% [CI, −3.7 to −0.1] in the 80–84 age group. The APC was 9.2% [CI, 3.6 to 24.8] from 2004 to 2008. From 2016–2018, APCs in 50–54 and 60–64 age groups are 13.4% [CI, 3.6 to 20.4] and 13.7% [CI, 0.4 to 23.6], respectively. Mortality rate ranged from 7.3 to 9.2 per 100,000 from 2009 to 2022, with a 4.9% [CI, 2.1 to 11.6] increase in 2009–2014 and a 1.9%–1.9%[CI, 4.4 to −0.6] decrease in 2014–2022. The incidence rate of prostate cancer in Türkiye increased until 2008, but then stabilised with the rates rising at the age of 50–54 and decreasing at the age of 80–84 years. Mortality rates initially increased but declined in the last 8 years. Further research is needed to explore factors influencing these trends.

前列腺癌是一个重大的全球健康问题，在发病率和死亡率方面存在很大的区域差异。在日本，它是第二大常见癌症，也是男性癌症相关死亡的第四大原因。本研究旨在分析日本前列腺癌发病率和死亡率的趋势。通过使用来自 rkiye癌症统计报告的发病率数据和来自TurkStat的死亡率数据，分析了 rkiye癌症统计报告的前列腺癌趋势。采用关节点回归分析发病率和死亡率的趋势，评估年平均百分比变化和年百分比变化（APC）。从2004年到2018年，年龄标准化前列腺癌发病率从24.9 / 10万上升到40.3 / 10万，其中75岁及以上人群发病率最高。总体而言，年平均百分比变化（AAPC）为2.6%[CI， 1.1至4.3]，50-54岁年龄组的具体比率为2.3% [CI， 0.5至3.5]，80-84岁年龄组的具体比率为- 1.9% [CI, - 3.7至- 0.1]。2004 - 2008年APC为9.2% [CI, 3.6 ~ 24.8]。2016-2018年，50-54岁和60-64岁年龄组的apc分别为13.4% [CI, 3.6 - 20.4]和13.7% [CI, 0.4 - 23.6]。2009年至2022年，死亡率为每10万人7.3至9.2人，2009 - 2014年上升4.9% [CI， 2.1至11.6]，2014-2022年下降1.9%-1.9% [CI， 4.4至- 0.6]。日本人前列腺癌的发病率在2008年之前一直在上升，但随后趋于稳定，在50-54岁时发病率上升，在80-84岁时发病率下降。死亡率最初有所上升，但在过去8年中有所下降。需要进一步的研究来探索影响这些趋势的因素。

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