Seminars in oncology最新文献_第2页

Comparative efficacy of osimertinib with and without radiation therapy in EGFR-mutated nonsmall cell lung cancer with brain metastases 奥西替尼加放疗和不加放疗治疗egfr突变非小细胞肺癌伴脑转移的比较疗效

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-11-02 DOI: 10.1016/j.seminoncol.2025.152436

Rafi Aibani , Jennifer Collins , Amir-Kabirian Borna , Amir Kamran

Brain metastases are common in patients with EGFR-mutant nonsmall cell lung cancer (NSCLC), yet optimal management remains under investigation. Osimertinib has demonstrated central nervous system (CNS) activity, but the added benefit of combining it with upfront local therapy is unclear. This study evaluated the comparative efficacy of osimertinib alone versus in combination with radiation therapy (RT) or stereotactic radiosurgery (SRS) in patients with EGFR-mutant NSCLC and brain metastases. We conducted a retrospective cohort study using the TriNetX Research Network, identifying adult patients diagnosed between 2010 and 2024 with EGFR-mutant NSCLC and brain metastases who received osimertinib. Patients were grouped into those who received RT or SRS within 6 months of starting osimertinib (cohort 1) and those who received osimertinib alone (cohort 2). Propensity score matching (1:1) was used to balance baseline characteristics. The primary outcome was 3-year survival; secondary outcomes included CNS complications, healthcare utilization, and second-line therapy initiation. Among 743 eligible patients, 217 in each cohort were matched. Three-year survival was significantly higher in cohort 1 (43% v 29%; HR 0.67, P = .003). Median survival was 25 months v 16 months, respectively. CNS complication rates were not significantly different overall, though sensitivity analysis excluding prior CNS history showed increased complications with osimertinib alone (HR 2.0, P = .007). SRS was independently associated with reduced mortality (HR 0.49, P = .003). Upfront local therapy with osimertinib may improve survival in EGFR-mutant NSCLC with brain metastases, though careful patient selection is warranted.

脑转移在egfr突变的非小细胞肺癌（NSCLC）患者中很常见，但最佳治疗方法仍在研究中。奥西替尼已经显示出中枢神经系统（CNS）的活性，但将其与前期局部治疗联合使用的额外益处尚不清楚。本研究评估了奥西替尼单独与联合放疗（RT）或立体定向放射手术（SRS）治疗egfr突变的非小细胞肺癌和脑转移患者的比较疗效。我们使用TriNetX研究网络进行了一项回顾性队列研究，确定了2010年至2024年间诊断为egfr突变型NSCLC和脑转移的成年患者，这些患者接受了奥西替尼。患者被分为在开始使用奥西替尼后6个月内接受RT或SRS的患者（队列1）和单独使用奥西替尼的患者（队列2）。倾向评分匹配（1:1）用于平衡基线特征。主要终点为3年生存率；次要结局包括中枢神经系统并发症、医疗保健利用和二线治疗开始。在743例符合条件的患者中，每个队列匹配217例。队列1的3年生存率显著提高（43% vs 29%; HR 0.67, P = 0.003）。中位生存期分别为25个月和16个月。CNS并发症发生率总体上无显著差异，但排除既往CNS病史的敏感性分析显示，单独使用奥西替尼会增加并发症（HR 2.0, P = .007）。SRS与死亡率降低独立相关（HR 0.49, P = 0.003）。奥西替尼的前期局部治疗可能提高egfr突变NSCLC脑转移患者的生存率，但需要谨慎选择患者。

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引用次数: 0

The role of circular RNAs in driving cancer advancement in low-oxygen conditions 环状rna在低氧条件下驱动癌症进展中的作用

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-10-30 DOI: 10.1016/j.seminoncol.2025.152435

Hamza Abu Owida , Raed Obaid Saleh , Suleiman Ibrahim Mohammad , Asokan Vasudevan , Roopashree R , Aditya Kashyap , Anima Nanda , Subhashree Ray , Ahmed Hussein , Hatif Abdulrazaq Yasin

Oxygen shortage, or hypoxia, is a unifying feature of solid tumors that broadly characterizes cancer biology and therapeutic outcome. In expanding tumors, cells adapt to low oxygen tensions by undergoing extensive metabolic reorganization, which is mainly orchestrated by hypoxia-inducible factor-1α (HIF-1α). The adaptive response initiates epithelial–mesenchymal transition (EMT), promotes metastatic dissemination, and facilitates the formation of cancer stem-like states that drive therapy resistance. Apart from such cellular reorganization, hypoxia also affects circular RNA (circRNA) biogenesis and function, a unique category of non-coding RNAs. CircRNAs are deposited into the tumor microenvironment to function as gene-expression regulators and signaling cascade modulators that are critical for survival, invasion, and drug resistance. Their unique hypoxia-associated expression patterns render them the first choice for diagnosis and prognosis. In this work, we examine the intricate relationship between circRNAs and hypoxia as well as associated molecular mechanisms. We also emphasize their role as ceRNAs, about microRNA binding and RNA-binding proteins, and their oncogenic role. Finally, we underscore the potential of targeting hypoxia-responsive circRNAs as novel therapeutic strategies for cancer.

氧缺乏或缺氧是实体肿瘤的一个统一特征，广泛表征了癌症生物学和治疗结果。在扩大的肿瘤中，细胞通过进行广泛的代谢重组来适应低氧紧张，这主要是由缺氧诱导因子-1α (HIF-1α)协调的。适应性反应启动上皮-间质转化（EMT），促进转移性传播，并促进癌症干细胞样状态的形成，从而驱动治疗耐药性。除了这种细胞重组外，缺氧还会影响环状RNA （circRNA）的生物发生和功能，环状RNA是一类独特的非编码RNA。CircRNAs沉积在肿瘤微环境中，作为基因表达调节剂和信号级联调节剂，对生存、侵袭和耐药至关重要。其独特的缺氧相关表达模式使其成为诊断和预后的首选。在这项工作中，我们研究了环状rna与缺氧之间的复杂关系以及相关的分子机制。我们还强调了它们作为cerna的作用，关于microRNA结合和rna结合蛋白，以及它们的致癌作用。最后，我们强调了靶向低氧应答环状rna作为癌症新治疗策略的潜力。

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引用次数: 0

Nanoparticle-based approaches for doxorubicin delivery in hepatocellular carcinoma: Current strategies and emerging innovations 基于纳米颗粒的肝细胞癌阿霉素递送方法：当前策略和新兴创新

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-10-30 DOI: 10.1016/j.seminoncol.2025.152434

Ali G. Alkhathami , Abdulrahman T. Ahmed , Ahmed Hussn , S. RenukaJyothi , Rajashree Panigrahi , Hussein Riyadh Abdul Kareem Al-Hetty , Hansi Negi , Pushkar Jassal , Fathi Jihad Hammady , Salah Abdulhadi Salih

Globally, hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related death, but HCC treatment with the chemotherapeutic doxorubicin is limited because of acquired drug resistance. In this review, we examined current knowledge on the specific molecular mechanisms of doxorubicin resistance in HCC, including overexpression of drug efflux (ABC family) transporters, aberrations of the drug target topoisomerase IIα (TOP2A), impairments in apoptosis (p53, FOXO3, Bcl-2 family members), oncogenic activation of pro-survival signaling pathways (NF-κB, PI3K/Akt, and MAPKs), instances of tumor heterogeneity with sirtuins, and cancer stem cells. Additionally, we investigate the role of non-coding RNAs, particularly microRNAs and long non-coding RNAs, in modulating sensitivity to and resistance to doxorubicin in HCC. In conclusion, nanomedicine will become crucial in overcoming the limitations of significant doxorubicin resistance in HCC, utilizing advanced mechanisms to modulate treatment with doxorubicin in this context. This review details various nanotechnology-based approaches to the delivery of doxorubicin, including passive targeting using the enhanced permeability and retention (EPR) effect, active targeting with specific ligands, and stimulus-responsive drug release in the tumor microenvironment (e.g., pH, redox potential). We focus on preclinical studies that utilized a variety of nanoparticle formulations for palliative care to patients with HCC, have investigated the use of liposomes, polymeric nanoparticles (e.g., PCL, chitosan), metallic particles (e.g., gold, silver, iron oxide), dendrimers, and metal-organic frameworks (MOFs), which have been loaded with doxorubicin or combined with other agents (e.g., cantharidin, berberine, isoginkgetin, ginger extract). The nanoparticle formulations enhanced drug delivery, increased drug accumulation per cell, reduced systemic toxicity, and overcame drug resistance mechanisms in HCC models.

在全球范围内，肝细胞癌（HCC）是癌症相关死亡的最常见原因之一，但由于获得性耐药，使用化疗药物阿霉素治疗HCC受到限制。在这篇综述中，我们研究了目前关于HCC中阿霉素耐药的特定分子机制的知识，包括药物外排（ABC家族）转运蛋白的过表达、药物靶点拓扑异构酶IIα (TOP2A)的畸变、细胞凋亡的损伤（p53、FOXO3、Bcl-2家族成员）、促生存信号通路（NF-κB、PI3K/Akt和MAPKs）的致癌激活、sirtuins的肿瘤异质性以及癌症干细胞。此外，我们还研究了非编码rna，特别是microrna和长链非编码rna在HCC中对阿霉素的敏感性和耐药性调节中的作用。总之，纳米药物在克服肝细胞癌中阿霉素耐药性的局限性方面将变得至关重要，在这种情况下，利用先进的机制来调节阿霉素的治疗。这篇综述详细介绍了各种基于纳米技术的阿霉素递送方法，包括利用增强渗透性和滞留性（EPR）效应的被动靶向，特定配体的主动靶向，以及肿瘤微环境中刺激反应性药物释放（例如pH值，氧化还原电位）。我们专注于临床前研究，利用各种纳米颗粒配方对HCC患者进行姑且治疗，研究了脂质体、聚合纳米颗粒（如PCL、壳聚糖）、金属颗粒（如金、银、氧化铁）、树形大分子和金属有机框架（mof）的使用，这些材料已加载阿霉素或与其他药物（如斑蝥素、小檗碱、异黄芪素、生姜提取物）联合使用。在HCC模型中，纳米颗粒制剂增强了药物传递，增加了每个细胞的药物积累，降低了全身毒性，并克服了耐药机制。

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引用次数: 0

Submicron silica particles drives prostate cancer aggressiveness via lipid-metabolic reprogramming 亚微米二氧化硅颗粒通过脂质代谢重编程驱动前列腺癌的侵袭性。

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-10-30 DOI: 10.1016/j.seminoncol.2025.152433

Pengpeng Su , Qianfeng Xu , Yan Wang , Wenjie Xie , Jundong Lin , Yangjia Zhuo , Jianheng Ye , Jianming Lu , Zhaodong Han , Fen Zou , Qishan Dai , Weide Zhong

Micron-sized (1 µm - 100 µm) and submicron-sized (100 nm–1 µm) silica particles are prevalent in both natural environments and areas influenced by human activities. Their environmental forms, origins, and pathways of human exposure differ markedly from those of nanoscale silica. Empirical studies have demonstrated that silica can induce cellular oxidative stress and mitochondrial dysfunction, as well as inhibit the activity of key enzymes in the tricarboxylic acid (TCA) cycle, such as isocitrate dehydrogenase. This inhibition can promote tumor cell proliferation and invasion. Furthermore, silica may activate the HIF-1α/mTOR signaling axis, leading to the upregulation of glucose transporter GLUT1 and lactate dehydrogenase (LDHA), thereby enhancing glycolytic metabolic flux. Concurrently, it may inhibit fatty acid β-oxidation, resulting in abnormal lipid accumulation and the promotion of pro-inflammatory mediator release. In summary, the accumulation of submicron silica within the bodies of cancer patients has the potential to induce metabolic disorders. Such metabolic reprogramming may influence the progression of prostate cancer (PCa) and adversely impact postoperative quality of life. In this study, we demonstrated that prolonged exposure of the lungs to submicron silica particles can induce alterations in lipid metabolism in PCa and significantly enhance the proliferation and invasive capacity of PCa cells. Consequently, elucidating the mechanisms underlying silica-induced metabolic imbalance holds substantial clinical significance for enhancing the prognosis of patients with tumors related to exposure.

微米尺寸（1微米- 100微米）和亚微米尺寸（100纳米-1微米）的二氧化硅颗粒普遍存在于自然环境和受人类活动影响的地区。它们的环境形式、来源和人类暴露途径与纳米级二氧化硅明显不同。实证研究表明，二氧化硅可以诱导细胞氧化应激和线粒体功能障碍，并抑制三羧酸（TCA）循环中关键酶的活性，如异柠檬酸脱氢酶。这种抑制作用可以促进肿瘤细胞的增殖和侵袭。此外，二氧化硅可能激活HIF-1α/mTOR信号轴，导致葡萄糖转运蛋白GLUT1和乳酸脱氢酶（LDHA）的上调，从而增强糖酵解代谢通量。同时，它可能抑制脂肪酸β-氧化，导致异常脂质积累，促进促炎介质释放。总之，亚微米二氧化硅在癌症患者体内的积累有可能诱发代谢紊乱。这种代谢重编程可能影响前列腺癌（PCa）的进展，并对术后生活质量产生不利影响。在这项研究中，我们证明了长时间暴露于亚微米二氧化硅颗粒的肺部可以诱导前列腺癌的脂质代谢改变，并显著增强前列腺癌细胞的增殖和侵袭能力。因此，阐明二氧化硅诱导的代谢失衡机制对于改善暴露相关肿瘤患者的预后具有重要的临床意义。

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引用次数: 0

Machine learning-based integration develops a lactate metabolism related gene signature for improving outcomes in pancreatic ductal adenocarcinoma 基于机器学习的整合开发了乳酸代谢相关基因标记，以改善胰腺导管腺癌的预后。

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-10-28 DOI: 10.1016/j.seminoncol.2025.152428

Wan-Li Ge , Chao-Qun Hou , Qing-Qing Zong , Dan-Rui Li , Yun-Peng Peng , Qiang Li

Objectives

Given its high global mortality rate, pancreatic ductal adenocarcinoma (PDAC) remains a significant area of investigation. However, a robust gene signature linked to lactate metabolism for PDAC patients has not yet been established. Our objective was therefore to construct a novel lactate metabolism related gene signature (LMRGS) capable of predicting patient outcomes and informing therapeutic decisions.

Methods

Genes associated with lactate metabolism were sourced from the Molecular Signatures Database (MsigDB). The LMRGS was constructed using distinct algorithmic combinations and its performance was subsequently verified in 8 separate patient cohorts. Multiomics analyses were employed to evaluate the signature’s impact on biological functions and to investigate its relationship with the immune microenvironment. EdU, colony formation and wound-healing assays were used to demonstrate the effects of lactate on pancreatic cancer cells.

Results

An artificial intelligence framework enabled the creation of an LMRGS that serves as an independent prognostic predictor for individuals with PDAC. This signature demonstrated considerable accuracy in forecasting overall survival. When patients were stratified into high- and low-risk groups, the high-risk group showed reduced immune cell infiltration and a poorer response to immunotherapy. Further investigation confirmed a strong correlation between the LMRGS and the immune milieu in PDAC. In vitro experiments demonstrated that lactate promotes the proliferation and migration of pancreatic cancer cells.

Conclusion

We have formulated a new LMRGS for PDAC which holds potential for informing personalized treatment plans. Interventions aimed at the lactate metabolic pathway could represent a promising strategy to boost therapeutic effectiveness and extend survival for patients diagnosed with this disease.

鉴于其全球高死亡率，胰腺导管腺癌（PDAC）仍然是一个重要的研究领域。然而，与PDAC患者乳酸代谢相关的强大基因特征尚未建立。因此，我们的目标是构建一种新的乳酸代谢相关基因标记（LMRGS），能够预测患者的预后并为治疗决策提供信息。方法：乳酸代谢相关基因来源于分子特征数据库（MsigDB）。LMRGS使用不同的算法组合构建，其性能随后在8个单独的患者队列中得到验证。采用多组学分析来评估该特征对生物功能的影响，并研究其与免疫微环境的关系。用EdU、菌落形成和伤口愈合实验来证明乳酸对胰腺癌细胞的影响。结果：人工智能框架能够创建LMRGS，作为PDAC患者的独立预后预测器。这一特征在预测总生存率方面显示出相当高的准确性。将患者分为高危组和低危组时，高危组免疫细胞浸润减少，对免疫治疗反应较差。进一步的研究证实了LMRGS与PDAC的免疫环境之间有很强的相关性。体外实验表明，乳酸促进胰腺癌细胞的增殖和迁移。结论：我们制定了一种新的PDAC LMRGS，具有指导个性化治疗方案的潜力。针对乳酸代谢途径的干预措施可能是一种有希望的策略，可以提高治疗效果，延长诊断为这种疾病的患者的生存期。

{"title":"Machine learning-based integration develops a lactate metabolism related gene signature for improving outcomes in pancreatic ductal adenocarcinoma","authors":"Wan-Li Ge , Chao-Qun Hou , Qing-Qing Zong , Dan-Rui Li , Yun-Peng Peng , Qiang Li","doi":"10.1016/j.seminoncol.2025.152428","DOIUrl":"10.1016/j.seminoncol.2025.152428","url":null,"abstract":"<div><h3>Objectives</h3><div>Given its high global mortality rate, pancreatic ductal adenocarcinoma (PDAC) remains a significant area of investigation. However, a robust gene signature linked to lactate metabolism for PDAC patients has not yet been established. Our objective was therefore to construct a novel lactate metabolism related gene signature (LMRGS) capable of predicting patient outcomes and informing therapeutic decisions.</div></div><div><h3>Methods</h3><div>Genes associated with lactate metabolism were sourced from the Molecular Signatures Database (MsigDB). The LMRGS was constructed using distinct algorithmic combinations and its performance was subsequently verified in 8 separate patient cohorts. Multiomics analyses were employed to evaluate the signature’s impact on biological functions and to investigate its relationship with the immune microenvironment. EdU, colony formation and wound-healing assays were used to demonstrate the effects of lactate on pancreatic cancer cells.</div></div><div><h3>Results</h3><div>An artificial intelligence framework enabled the creation of an LMRGS that serves as an independent prognostic predictor for individuals with PDAC. This signature demonstrated considerable accuracy in forecasting overall survival. When patients were stratified into high- and low-risk groups, the high-risk group showed reduced immune cell infiltration and a poorer response to immunotherapy. Further investigation confirmed a strong correlation between the LMRGS and the immune milieu in PDAC. In vitro experiments demonstrated that lactate promotes the proliferation and migration of pancreatic cancer cells.</div></div><div><h3>Conclusion</h3><div>We have formulated a new LMRGS for PDAC which holds potential for informing personalized treatment plans. Interventions aimed at the lactate metabolic pathway could represent a promising strategy to boost therapeutic effectiveness and extend survival for patients diagnosed with this disease.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"53 1","pages":"Article 152428"},"PeriodicalIF":2.5,"publicationDate":"2025-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145401775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 nervous system in prostate cancer: A basic science and clinical perspective 前列腺癌的神经系统：基础科学和临床观点

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-10-24 DOI: 10.1016/j.seminoncol.2025.152425

Dawid Sigorski , Anna Kasprzyk-Pawelec , Maciej Michalak , Roman Sosnowski , Michał M. Hryciuk , Aleksandra Sejda , Jacek Gulczyński , Joanna Kitlinska , Sergiusz Nawrocki , Ewa Iżycka-Świeszewska

Prostate cancer (PCa) constitutes an important health challenge worldwide. The nervous system, in a complex and multimodal manner, regulates prostate physiology and PCa development and affects the course of the disease. The phenomena of axonogenesis and neurogenesis, first described in PCa, were a breakthrough discovery that changed our understanding of cancer-nerve crosstalk. Different nerve types within the cancer stroma and tumor surroundings create complex interactions between the cancer microenvironment elements based on neurotransmission, affecting the hallmarks of cancer. The most common form of PCa and nerve interaction is the perineural invasion (PNI), which recently has been suggested as a driver of metastases. Additionally, many preclinical discoveries depict the molecular mechanisms of altered nerve activity, showing the pivotal role of sympathetic and parasympathetic signaling systems in localized and advanced PCa, axon-guidance molecules and neurotrophin. The neuroendocrine switch in advanced PCa is one of reasons of lethal, castration-resistant phase of the disease. Knowledge about the infiltration status of the periprostatic nerves present in radiological imaging is important for urologists in planning the treatment. Although some studies suggest that PNI and nerve density may be prognostic factors in PCa, it is necessary to evaluate these indicators better and apply them to practice. The neural-based therapeutic application in PCa is limited currently. Some studies showed that β blockers reduce PCa-specific mortality and neuroendocrine differentiation potential. This review provides a comprehensive, up-to date synthesis of PCa neurobiology, uniquely integrating both preclinial and clinical perspectives.

前列腺癌（PCa）是世界范围内一个重要的健康挑战。神经系统以复杂和多模式的方式调节前列腺生理和前列腺癌的发展，并影响疾病的病程。在PCa中首次描述的轴突发生和神经发生现象是一个突破性的发现，改变了我们对癌症-神经串扰的理解。肿瘤基质和肿瘤环境中不同类型的神经在基于神经传递的癌症微环境元素之间产生复杂的相互作用，影响癌症的特征。前列腺癌与神经相互作用最常见的形式是神经周围浸润（PNI），最近被认为是转移的驱动因素。此外，许多临床前发现描述了神经活动改变的分子机制，显示了交感和副交感信号系统在局部和晚期PCa、轴突引导分子和神经营养蛋白中的关键作用。晚期前列腺癌的神经内分泌开关是该疾病致死性、去势抵抗期的原因之一。了解前列腺周围神经的浸润状况，在放射成像是重要的泌尿科医生在计划治疗。虽然一些研究表明PNI和神经密度可能是前列腺癌的预后因素，但有必要更好地评估这些指标并将其应用于实践。目前基于神经的治疗在PCa中的应用是有限的。一些研究表明β受体阻滞剂可降低pca特异性死亡率和神经内分泌分化潜能。这篇综述提供了一个全面的，最新的PCa神经生物学合成，独特地整合了临床前和临床的观点。

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引用次数: 0

Physics-informed deep learning sharpens nano diagnostics for elusive pancreatic cancer 基于物理学的深度学习使难以捉摸的胰腺癌的纳米诊断更加清晰

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-10-22 DOI: 10.1016/j.seminoncol.2025.152427

Abbas Rahdar , Vahideh Mhammadzadeh , Sobia Razzaq , Maryam Shirzad , Sonia Fathi-karkan , Ali Bakhshi , Razieh Behzadmehr , Zelal Kharaba , Luiz Fernando Romanholo Ferreira

Pancreatic disease affects over 10% of the world population, and the most dangerous is pancreatic cancer (PC). The disease is mostly of late age of onset, especially in developed countries, and is associated with poor prognosis due to late presentation. Present screening tests like imaging and biomarkers are insensitive for the high-risk group. Invasive and noninvasive imaging modalities are other diagnostic tests with variable accuracy and accompanying risks. Chemotherapy and surgery are the first lines of treatment, but only 15%–20% of patients are eligible for surgery and the rate of recurrence is very high. Emerging technologies, including physics-informed deep learning (PIDL) and artificial intelligence (AI), are improving early detection techniques by evaluating images and synthesizing data more efficiently. Nanomedicine and AI-driven radiomics are individualizing diagnoses, enhancing drug delivery, and tackling tumor microenvironment issues. Hybrid model methodologies are improving prediction precision in oncology research, while computational drug development and liquid biopsy technologies enable early diagnosis and personalized treatment. The amalgamation of AI, imaging, nanomedicine, and physics-informed models has the potential to transform PC diagnostics, enhancing early detection and patient prognoses.

胰腺疾病影响着超过10%的世界人口，其中最危险的是胰腺癌（PC）。该病大多发病较晚，特别是在发达国家，由于发病较晚，预后较差。目前的筛查测试，如成像和生物标志物对高危人群不敏感。侵入性和非侵入性成像方式是另一种诊断测试，具有不同的准确性和伴随的风险。化疗和手术是治疗的第一线，但只有15%-20%的患者符合手术条件，复发率很高。包括基于物理的深度学习（PIDL）和人工智能（AI）在内的新兴技术正在通过更有效地评估图像和合成数据来改进早期检测技术。纳米医学和人工智能驱动的放射组学正在个性化诊断、增强药物输送和解决肿瘤微环境问题。混合模型方法正在提高肿瘤研究的预测精度，而计算药物开发和液体活检技术使早期诊断和个性化治疗成为可能。人工智能、成像、纳米医学和物理信息模型的融合有可能改变PC诊断，增强早期检测和患者预后。

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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 : 2025-10-04 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

Deciphering autophagy signaling in cancer: A paradigm shift from molecular classifications to clinical innovations. 解读癌症中的自噬信号：从分子分类到临床创新的范式转变。

IF 2.5 3区医学 Q2 ONCOLOGY

Seminars in oncology

Pub Date : 2025-10-01 Epub Date: 2025-08-08 DOI: 10.1016/j.seminoncol.2025.152397

Farag M A Altalbawy, Ehab Yassen Theab, Gaurav Sanghvi, R Roopashree, Aditya Kashyap, Hussein Riyadh Abdul Kareem Al-Hetty, S Gayathri, Rajashree Panigrahi, Yasser Fakri Mustafa, Hatif Abdulrazaq Yasin

The intracellular breakdown process known as autophagy occurs when cells experience adverse conditions, such as organelle damage, the presence of abnormal proteins, hypoxia stress, low energy levels, or nutritional deprivation. The autophagic process begins by forming autophagosomes, which then merge with lysosomes to recycle degraded materials. Autophagy functions in multiple ways to affect cancer development and treatment outcomes. Tumor cells with low autophagy levels may exhibit anti-tumor effects during cancer initiation because their connection to malignant transformation is possible. The promotion of autophagy appears beneficial for cancer prevention in this context. The survival of cancer cells through increased autophagy enables tumor growth in existing tumors by allowing them to overcome metabolic and treatment-related challenges. Research indicates that blocking autophagy through the use of drugs or genetic methods makes cancer cells more susceptible to chemotherapy, radiation, and targeted therapies, suggesting that inhibiting the autophagic system may be a promising approach to enhance treatment. Excessive autophagy activation could be a therapeutic approach to manage cancer cells that resist cell death. The successful treatment of cancer requires an understanding of autophagy's dual nature. This review examines potential therapeutic strategies for tumors by analyzing autophagy-related signaling pathways and the essential factors that influence cancer development.

当细胞经历不利条件时，如细胞器损伤、异常蛋白的存在、缺氧应激、低能量水平或营养剥夺，细胞内分解过程即自噬发生。自噬过程始于形成自噬体，然后自噬体与溶酶体结合以回收降解物质。自噬以多种方式影响癌症的发展和治疗结果。低自噬水平的肿瘤细胞可能在癌变过程中表现出抗肿瘤作用，因为它们可能与恶性转化有关。在这种情况下，促进自噬似乎有利于预防癌症。癌细胞通过增加的自噬存活，使现有肿瘤能够克服代谢和治疗相关的挑战，从而使肿瘤生长。研究表明，通过药物或遗传方法阻断自噬使癌细胞更容易受到化疗、放疗和靶向治疗的影响，这表明抑制自噬系统可能是一种有希望的增强治疗的方法。过度自噬激活可能是一种治疗方法来管理癌细胞抵抗细胞死亡。癌症的成功治疗需要了解自噬的双重性质。本文通过分析自噬相关信号通路和影响肿瘤发展的重要因素来探讨肿瘤的潜在治疗策略。

{"title":"Deciphering autophagy signaling in cancer: A paradigm shift from molecular classifications to clinical innovations.","authors":"Farag M A Altalbawy, Ehab Yassen Theab, Gaurav Sanghvi, R Roopashree, Aditya Kashyap, Hussein Riyadh Abdul Kareem Al-Hetty, S Gayathri, Rajashree Panigrahi, Yasser Fakri Mustafa, Hatif Abdulrazaq Yasin","doi":"10.1016/j.seminoncol.2025.152397","DOIUrl":"10.1016/j.seminoncol.2025.152397","url":null,"abstract":"<p><p>The intracellular breakdown process known as autophagy occurs when cells experience adverse conditions, such as organelle damage, the presence of abnormal proteins, hypoxia stress, low energy levels, or nutritional deprivation. The autophagic process begins by forming autophagosomes, which then merge with lysosomes to recycle degraded materials. Autophagy functions in multiple ways to affect cancer development and treatment outcomes. Tumor cells with low autophagy levels may exhibit anti-tumor effects during cancer initiation because their connection to malignant transformation is possible. The promotion of autophagy appears beneficial for cancer prevention in this context. The survival of cancer cells through increased autophagy enables tumor growth in existing tumors by allowing them to overcome metabolic and treatment-related challenges. Research indicates that blocking autophagy through the use of drugs or genetic methods makes cancer cells more susceptible to chemotherapy, radiation, and targeted therapies, suggesting that inhibiting the autophagic system may be a promising approach to enhance treatment. Excessive autophagy activation could be a therapeutic approach to manage cancer cells that resist cell death. The successful treatment of cancer requires an understanding of autophagy's dual nature. This review examines potential therapeutic strategies for tumors by analyzing autophagy-related signaling pathways and the essential factors that influence cancer development.</p>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"152397"},"PeriodicalIF":2.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

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 : 2025-09-30 DOI: 10.1016/j.seminoncol.2025.152424

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

引用次数: 0