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Targeting endothelial cell anergy to improve CAR T cell therapy for solid tumors 以内皮细胞过敏为靶点,改进治疗实体瘤的 CAR T 细胞疗法。
IF 9.7 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-07-15 DOI: 10.1016/j.bbcan.2024.189155

Chimeric antigen receptor (CAR) T cell therapy presents significant results, especially for the treatment of hematologic malignancies. However, there are limitations and challenges to be overcome to achieve similar success for the treatment of solid tumors. These challenges involve selection of the target, infiltration into the tumor microenvironment and maintenance of functionality. The tumor vasculature is a major barrier for leukocytes to enter the tumor parenchyma. Due to the exposure of the vasculature to angiogenic growth factors during tumor progression, the endothelial cells become anergic to inflammatory cytokines, resulting in reduced leukocyte adhesion molecule expression. As such adhesion molecules are a prerequisite for leukocyte extravasation, endothelial cell anergy allows tumors to escape from endogenous immunity, as well as from cellular immunotherapies such as CAR T cells. Hence, overcoming endothelial cell anergy, e.g. through the administration of angiogenesis inhibitors, is believed to restore anti-tumor immunity. Concomitantly, both endogenous immune cells as well as cellular therapeutics such as CAR T cells can permeate into the tumor parenchyma. Here, we discuss how prior or concomitant treatment with an antiangiogenic drug can improve CAR T cell therapy, to become an attractive strategy for the treatment of solid tumors.

嵌合抗原受体(CAR)T细胞疗法效果显著,尤其是在治疗血液系统恶性肿瘤方面。然而,要在实体瘤治疗中取得类似的成功,还需要克服一些限制和挑战。这些挑战涉及靶点的选择、肿瘤微环境的渗透和功能的维持。肿瘤血管是白细胞进入肿瘤实质的主要屏障。在肿瘤进展过程中,由于血管暴露于血管生成生长因子,内皮细胞对炎症细胞因子过敏,导致白细胞粘附分子表达减少。由于这种粘附分子是白细胞外渗的先决条件,内皮细胞过敏使肿瘤得以逃避内源性免疫以及 CAR T 细胞等细胞免疫疗法。因此,通过使用血管生成抑制剂等方法克服内皮细胞凋亡,被认为可以恢复抗肿瘤免疫力。同时,内源性免疫细胞和细胞疗法(如 CAR T 细胞)都可以渗透到肿瘤实质中。在此,我们将讨论如何通过事先或同时使用抗血管生成药物来改善 CAR T 细胞疗法,使其成为治疗实体瘤的一种有吸引力的策略。
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引用次数: 0
Reactive oxygen species of tumor microenvironment: Harnessing for immunogenic cell death 肿瘤微环境中的活性氧:利用免疫原性细胞死亡。
IF 9.7 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-07-15 DOI: 10.1016/j.bbcan.2024.189154

The tumor microenvironment (TME) is a dynamic and complex system that undergoes continuous changes in its network architecture, notably affecting redox homeostasis. These alterations collectively shape a diverse ecosystem actively supporting tumor progression by influencing the cellular and molecular components of the TME. Despite the remarkable clinical advancements in cancer immunotherapy, its spectrum of clinical utility is limited by the altered TME and inadequate tumor immunogenicity. Recent studies have revealed that some conventional and targeted therapy strategies can augment the efficacy of immunotherapy even in patients with less immunogenic solid tumors. These strategies provoke immunogenic cell death (ICD) through the ROS-dependent liberation of damage-associated molecular patterns (DAMPs). These DAMPs recognize and bind with Pattern Recognition Receptors (PRRs) on immune cells, activating and maturing defense cells, ultimately leading to a robust antitumor immune response. The present review underscores the pivotal role of redox homeostasis in orchestrating the transition of TME from a cold to a hot phenotype and the ROS-ICD axis in immune response induction. Additionally, it provides up-to-date insights into strategies that leverage ROS generation to induce ICD. The comprehensive analysis aims to develop ROS-based effective cancer immunotherapies for less immunogenic tumors.

肿瘤微环境(TME)是一个动态的复杂系统,其网络结构不断发生变化,特别是影响氧化还原平衡。这些变化共同形成了一个多样化的生态系统,通过影响肿瘤微环境的细胞和分子成分,积极支持肿瘤的进展。尽管癌症免疫疗法在临床上取得了令人瞩目的进展,但其临床应用范围仍受到 TME 改变和肿瘤免疫原性不足的限制。最近的研究发现,一些常规和靶向治疗策略可以增强免疫疗法的疗效,即使是免疫原性较低的实体瘤患者也不例外。这些策略通过依赖于 ROS 的损伤相关分子模式(DAMPs)的释放,引发免疫原性细胞死亡(ICD)。这些 DAMPs 可识别免疫细胞上的模式识别受体(PRRs)并与之结合,激活和成熟防御细胞,最终产生强大的抗肿瘤免疫反应。本综述强调了氧化还原平衡在协调 TME 从冷表型向热表型转变中的关键作用,以及 ROS-ICD 轴在诱导免疫反应中的关键作用。此外,它还提供了关于利用 ROS 生成诱导 ICD 的策略的最新见解。综合分析旨在为免疫原性较低的肿瘤开发基于 ROS 的有效癌症免疫疗法。
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引用次数: 0
New horizons in the mechanisms and therapeutic strategies for PD-L1 protein degradation in cancer 癌症中 PD-L1 蛋白降解机制和治疗策略的新视野。
IF 9.7 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-07-09 DOI: 10.1016/j.bbcan.2024.189152
Zhi Li , Xi Yu , Zeting Yuan , Lei Li , Peihao Yin

Programmed death-ligand 1 (PD-L1) has become a crucial focus in cancer immunotherapy considering it is found in many different cells. Cancer cells enhance the suppressive impact of programmed death receptor 1 (PD-1) through elevating PD-L1 expression, which allows them to escape immune detection. Although there have been significant improvements, the effectiveness of anti-PD-1/PD-L1 treatment is still limited to a specific group of patients. An important advancement in cancer immunotherapy involves improving the PD-L1 protein degradation. This review thoroughly examined the processes by which PD-L1 breaks down, including the intracellular pathways of ubiquitination-proteasome and autophagy-lysosome. In addition, the analysis revealed changes that affect PD-L1 stability, such as phosphorylation and glycosylation. The significant consequences of these procedures on cancer immunotherapy and their potential role in innovative therapeutic approaches are emphasised. Our future efforts will focus on understanding new ways in which PD-L1 degradation is controlled and developing innovative treatments, such as proteolysis-targeting chimeras designed specifically to degrade PD-L1. It is crucial to have a thorough comprehension of these pathways in order to improve cancer immunotherapy strategies and hopefully improve therapeutic effectiveness.

程序性死亡配体 1(PD-L1)存在于许多不同的细胞中,因此已成为癌症免疫疗法的一个重要焦点。癌细胞通过提高PD-L1的表达来增强程序性死亡受体1(PD-1)的抑制作用,从而逃避免疫检测。虽然抗PD-1/PD-L1治疗的效果有了明显改善,但仍仅限于特定的患者群体。癌症免疫疗法的一个重要进展是改善了 PD-L1 蛋白的降解。这篇综述深入研究了 PD-L1 的分解过程,包括泛素化-蛋白酶体和自噬-溶酶体等细胞内途径。此外,分析还揭示了影响 PD-L1 稳定性的变化,如磷酸化和糖基化。我们强调了这些过程对癌症免疫疗法的重大影响,以及它们在创新治疗方法中的潜在作用。我们今后的工作重点是了解控制 PD-L1 降解的新方法,并开发创新疗法,如专门设计用于降解 PD-L1 的蛋白水解靶向嵌合体。透彻了解这些途径对于改进癌症免疫疗法策略和提高治疗效果至关重要。
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引用次数: 0
Metabolomic biomarkers of multiple myeloma: A systematic review 多发性骨髓瘤的代谢组生物标志物:系统回顾
IF 9.7 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-07-08 DOI: 10.1016/j.bbcan.2024.189151

Multiple myeloma (MM) is an incurable malignancy of clonal plasma cells. Various diagnostic methods are used in parallel to accurately determine stage and severity of the disease. Identifying a biomarker or a panel of biomarkers could enhance the quality of medical care that patients receive by adopting a more personalized approach. Metabolomics utilizes high-throughput analytical platforms to examine the levels and quantities of biochemical compounds in biosamples. The aim of this review was to conduct a systematic literature search for potential metabolic biomarkers that may aid in the diagnosis and prognosis of MM. The review was conducted in accordance with PRISMA recommendations and was registered in PROSPERO. The systematic search was performed in PubMed, CINAHL, SciFinder, Scopus, The Cochrane Library and Google Scholar. Studies were limited to those involving people with clinically diagnosed MM and healthy controls as comparators. Articles had to be published in English and had no restrictions on publication date or sample type. The quality of articles was assessed according to QUADOMICS criteria. A total of 709 articles were collected during the literature search. Of these, 436 were excluded based on their abstract, with 26 more removed after a thorough review of the full text. Finally, 16 articles were deemed relevant and were subjected to further analysis of their data. A number of promising candidate biomarkers was discovered. Follow-up studies with large sample sizes are needed to determine their suitability for clinical applications.

多发性骨髓瘤是一种无法治愈的克隆性浆细胞恶性肿瘤。各种诊断方法并行使用,以准确确定疾病的分期和严重程度。确定一种或一组生物标志物,可以通过采用更加个性化的方法,提高患者接受医疗护理的质量。代谢组学利用高通量分析平台来检测生物样本中生化化合物的水平和数量。本综述旨在对可能有助于 MM 诊断和预后的潜在代谢生物标志物进行系统的文献检索。综述按照 PRISMA 建议进行,并在 PROSPERO 上进行了注册。在 PubMed、CINAHL、SciFinder、Scopus、The Cochrane Library 和 Google Scholar 中进行了系统检索。研究仅限于涉及临床确诊的 MM 患者和健康对照组的研究。文章必须以英语发表,对发表日期或样本类型没有限制。文章质量根据 QUADOMICS 标准进行评估。文献检索共收集到 709 篇文章。其中,436 篇文章根据其摘要被排除,另有 26 篇文章在对全文进行彻底审查后被删除。最后,有 16 篇文章被认为是相关的,并对其数据进行了进一步分析。发现了一些有希望的候选生物标志物。要确定这些生物标志物是否适合临床应用,还需要进行大样本量的后续研究。
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引用次数: 0
Small non-coding RNAs and pancreatic ductal adenocarcinoma: Linking diagnosis, pathogenesis, drug resistance, and therapeutic potential 小非编码 RNA 与胰腺导管腺癌:诊断、发病机制、耐药性和治疗潜力之间的联系。
IF 9.7 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-07-08 DOI: 10.1016/j.bbcan.2024.189153
Ryan N. Fuller , Ann Morcos , Joab Galvan Bustillos , David Caba Molina , Nathan R. Wall

This review comprehensively investigates the intricate interplay between small non-coding RNAs (sncRNAs) and pancreatic ductal adenocarcinoma (PDAC), a devastating malignancy with limited therapeutic options. Our analysis reveals the pivotal roles of sncRNAs in various facets of PDAC biology, spanning diagnosis, pathogenesis, drug resistance, and therapeutic strategies. sncRNAs have emerged as promising biomarkers for PDAC, demonstrating distinct expression profiles in diseased tissues. sncRNA differential expression patterns, often detectable in bodily fluids, hold potential for early and minimally invasive diagnostic approaches. Furthermore, sncRNAs exhibit intricate involvement in PDAC pathogenesis, regulating critical cellular processes such as proliferation, apoptosis, and metastasis. Additionally, mechanistic insights into sncRNA-mediated pathogenic pathways illuminate novel therapeutic targets and interventions. A significant focus of this review is dedicated to unraveling sncRNA mechanisms underlying drug resistance in PDAC. Understanding these mechanisms at the molecular level is imperative for devising strategies to overcome drug resistance. Exploring the therapeutic landscape, we discuss the potential of sncRNAs as therapeutic agents themselves as their ability to modulate gene expression with high specificity renders them attractive candidates for targeted therapy. In summary, this review integrates current knowledge on sncRNAs in PDAC, offering a holistic perspective on their diagnostic, pathogenic, and therapeutic relevance. By elucidating the roles of sncRNAs in PDAC biology, this review provides valuable insights for the development of novel diagnostic tools and targeted therapeutic approaches, crucial for improving the prognosis of PDAC patients.

本综述全面研究了小非编码 RNA(sncRNA)与胰腺导管腺癌(PDAC)之间错综复杂的相互作用。我们的分析揭示了 sncRNA 在 PDAC 生物学各方面的关键作用,包括诊断、发病机制、耐药性和治疗策略。sncRNA 已成为 PDAC 有希望的生物标记物,在患病组织中显示出独特的表达谱。sncRNA 的差异表达模式通常可在体液中检测到,为早期和微创诊断方法提供了潜力。此外,sncRNA 在 PDAC 发病机制中表现出复杂的参与性,可调节增殖、凋亡和转移等关键细胞过程。此外,对 sncRNA 介导的致病途径的机理研究也为新的治疗靶点和干预措施提供了启示。本综述的一个重点是揭示 PDAC 耐药的 sncRNA 机制。从分子水平了解这些机制对于制定克服耐药性的策略至关重要。在探讨治疗前景时,我们讨论了 sncRNA 本身作为治疗药物的潜力,因为 sncRNA 具有高度特异性调节基因表达的能力,使其成为有吸引力的候选靶向治疗药物。总之,这篇综述整合了目前有关 PDAC 中 sncRNAs 的知识,从整体角度探讨了它们在诊断、致病和治疗方面的相关性。通过阐明 sncRNAs 在 PDAC 生物学中的作用,本综述为开发新型诊断工具和靶向治疗方法提供了宝贵的见解,这对改善 PDAC 患者的预后至关重要。
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引用次数: 0
Exploring the impact of flavin homeostasis on cancer cell metabolism 探索黄素平衡对癌细胞代谢的影响。
IF 9.7 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-07-04 DOI: 10.1016/j.bbcan.2024.189149
Alessia Nisco , Maria Tolomeo , Mariafrancesca Scalise , Katia Zanier , Maria Barile

Flavins and their associated proteins have recently emerged as compelling players in the landscape of cancer biology. Flavins, encompassing flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), serve as coenzymes in a multitude of cellular processes, such as metabolism, apoptosis, and cell proliferation. Their involvement in oxidative phosphorylation, redox homeostasis, and enzymatic reactions has long been recognized. However, recent research has unveiled an extended role for flavins in the context of cancer. In parallel, riboflavin transporters (RFVTs), FAD synthase (FADS), and riboflavin kinase (RFK) have gained prominence in cancer research. These proteins, responsible for riboflavin uptake, FAD biosynthesis, and FMN generation, are integral components of the cellular machinery that governs flavin homeostasis. Dysregulation in the expression/function of these proteins has been associated with various cancers, underscoring their potential as diagnostic markers, therapeutic targets, and key determinants of cancer cell behavior. This review embarks on a comprehensive exploration of the multifaceted role of flavins and of the flavoproteins involved in nucleus-mitochondria crosstalk in cancer. We journey through the influence of flavins on cancer cell energetics, the modulation of RFVTs in malignant transformation, the diagnostic and prognostic significance of FADS, and the implications of RFK in drug resistance and apoptosis. This review also underscores the potential of these molecules and processes as targets for novel diagnostic and therapeutic strategies, offering new avenues for the battle against this relentless disease.

黄素及其相关蛋白最近在癌症生物学研究中崭露头角。黄素包括黄素单核苷酸(FMN)和黄素腺嘌呤二核苷酸(FAD),在新陈代谢、细胞凋亡和细胞增殖等多种细胞过程中充当辅酶。它们在氧化磷酸化、氧化还原平衡和酶促反应中的参与早已得到认可。然而,最近的研究揭示了黄素在癌症中的延伸作用。与此同时,核黄素转运体(RFVTs)、FAD 合成酶(FADS)和核黄素激酶(RFK)也在癌症研究中占据了重要地位。这些蛋白质负责核黄素摄取、FAD 生物合成和 FMN 生成,是控制黄素平衡的细胞机制的重要组成部分。这些蛋白的表达/功能失调与多种癌症有关,凸显了它们作为诊断标志物、治疗靶点和癌细胞行为关键决定因素的潜力。本综述将全面探讨黄素的多方面作用以及参与癌症中细胞核-线粒体串扰的黄素蛋白。我们将探讨黄素对癌细胞能量的影响、RFVTs 在恶性转化中的调节作用、FADS 的诊断和预后意义以及 RFK 在耐药性和细胞凋亡中的作用。这篇综述还强调了这些分子和过程作为新型诊断和治疗策略靶点的潜力,为对抗这种无情的疾病提供了新的途径。
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引用次数: 0
Histone deacetylase complexes: Structure, regulation and function 组蛋白去乙酰化酶复合物:结构、调节和功能
IF 9.7 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-07-04 DOI: 10.1016/j.bbcan.2024.189150
Moges Dessale Asmamaw , Ang He , Li-Rong Zhang , Hong-Min Liu , Ya Gao

Histone deacetylases (HDACs) are key epigenetic regulators, and transcriptional complexes with deacetylase function are among the epigenetic corepressor complexes in the nucleus that target the epigenome. HDAC-bearing corepressor complexes such as the Sin3 complex, NuRD complex, CoREST complex, and SMRT/NCoR complex are common in biological systems. These complexes activate the otherwise inactive HDACs in a solitary state. HDAC complexes play vital roles in the regulation of key biological processes such as transcription, replication, and DNA repair. Moreover, deregulated HDAC complex function is implicated in human diseases including cancer. Therapeutic strategies targeting HDAC complexes are being sought actively. Thus, illustration of the nature and composition of HDAC complexes is vital to understanding the molecular basis of their functions under physiologic and pathologic conditions, and for designing targeted therapies. This review presents key aspects of large multiprotein HDAC-bearing complexes including their structure, function, regulatory mechanisms, implication in disease development, and role in therapeutics.

组蛋白去乙酰化酶(HDAC)是关键的表观遗传调控因子,具有去乙酰化酶功能的转录复合物是细胞核中针对表观基因组的表观遗传核心抑制复合物之一。带有 HDAC 的核心抑制复合体,如 Sin3 复合体、NuRD 复合体、CoREST 复合体和 SMRT/NCoR 复合体,在生物系统中很常见。这些复合体能以单独状态激活原本不活跃的 HDAC。HDAC 复合物在转录、复制和 DNA 修复等关键生物过程的调控中发挥着重要作用。此外,HDAC 复合物功能失调还与包括癌症在内的人类疾病有关。目前正在积极寻找针对 HDAC 复合物的治疗策略。因此,说明 HDAC 复合物的性质和组成对于了解它们在生理和病理条件下发挥功能的分子基础以及设计靶向疗法至关重要。本综述介绍了大型多蛋白 HDAC 复合物的主要方面,包括其结构、功能、调控机制、在疾病发展中的影响以及在治疗中的作用。
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引用次数: 0
Role of cell division cycle-associated proteins in regulating cell cycle and promoting tumor progression 细胞分裂周期相关蛋白在调节细胞周期和促进肿瘤进展中的作用。
IF 9.7 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-30 DOI: 10.1016/j.bbcan.2024.189147

The cell division cycle-associated protein (CDCA) family is important in regulating cell division. High CDCA expression is significantly linked to tumor development. This review summarizes clinical and basic studies on CDCAs conducted in recent decades. Furthermore, it systematically introduces the molecular expression and function, key mechanisms, cell cycle regulation, and roles of CDCAs in tumor development, cell proliferation, drug resistance, invasion, and metastasis. Additionally, it presents the latest research on tumor diagnosis, prognosis, and treatment targeting CDCAs. These findings are pivotal for further in-depth studies on the role of CDCAs in promoting tumor development and provide theoretical support for their application as new anti-tumor targets.

细胞分裂周期相关蛋白(CDCA)家族在调节细胞分裂方面具有重要作用。CDCA 的高表达与肿瘤的发生发展密切相关。本综述总结了近几十年来有关 CDCA 的临床和基础研究。此外,它还系统地介绍了 CDCAs 的分子表达和功能、关键机制、细胞周期调控以及在肿瘤发生、细胞增殖、耐药性、侵袭和转移中的作用。此外,它还介绍了有关肿瘤诊断、预后和针对 CDCAs 治疗的最新研究。这些发现对进一步深入研究 CDCAs 在促进肿瘤发生发展中的作用至关重要,并为将 CDCAs 用作新的抗肿瘤靶点提供了理论支持。
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引用次数: 0
Pathophysiological role of histamine signaling and its implications in glioblastoma 组胺信号的病理生理学作用及其对胶质母细胞瘤的影响。
IF 9.7 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-30 DOI: 10.1016/j.bbcan.2024.189146
Poonam Yadav , Raghupathy Vengoji , Maneesh Jain , Surinder K. Batra , Nicole Shonka

Glioblastoma (GBM), an extremely aggressive and prevalent malignant brain tumor, remains a challenge to treat. Despite a multimodality treatment approach, GBM recurrence remains inevitable, particularly with the emergence of temozolomide (TMZ) resistance and limited treatment options. Surprisingly, previous studies show that a history of allergies, atopy, or asthma is inversely associated with GBM risk. Further, the electronic medical record at the University Hospital of Lausanne showed that the GBM patients taking antihistamine during treatment had better survival. Histamine is an essential neurotransmitter in the brain and plays a significant role in regulating sleep, hormonal balance, and cognitive functions. Elevated levels of histamine and increased histamine receptor expression have been found in different tumors and their microenvironments, including GBM. High histamine 1 receptor (HRH1) expression is inversely related to overall and progression-free survival in GBM patients, further emphasizing the role of histamine in disease progression. This review aims to provide insights into the challenges of GBM treatment, the role of histamine in GBM progression, and the rationale for considering antihistamines as targeted therapy. The review concludes by encouraging further investigation into antihistamine mechanisms and their impact on the tumor microenvironment.

胶质母细胞瘤(GBM)是一种侵袭性极强、发病率极高的恶性脑肿瘤,其治疗仍是一项挑战。尽管采用了多模式治疗方法,但 GBM 复发仍不可避免,尤其是在出现替莫唑胺(TMZ)耐药性和治疗选择有限的情况下。令人惊讶的是,以往的研究表明,过敏史、过敏症或哮喘与 GBM 风险成反比。此外,洛桑大学医院的电子病历显示,在治疗期间服用抗组胺药的GBM患者存活率更高。组胺是大脑中一种重要的神经递质,在调节睡眠、荷尔蒙平衡和认知功能方面发挥着重要作用。组胺水平升高和组胺受体表达增加已被发现存在于不同的肿瘤及其微环境中,包括脑胶质瘤。组胺 1 受体(HRH1)的高表达与 GBM 患者的总生存期和无进展生存期成反比,这进一步强调了组胺在疾病进展中的作用。本综述旨在深入探讨 GBM 治疗面临的挑战、组胺在 GBM 进展中的作用以及考虑将抗组胺药作为靶向治疗的理由。综述最后鼓励进一步研究抗组胺机制及其对肿瘤微环境的影响。
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引用次数: 0
Evolving treatment landscape in thymic epithelial tumors: From mechanism to therapy 胸腺上皮肿瘤治疗的演变:从机制到治疗。
IF 9.7 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1016/j.bbcan.2024.189145
Yehao Yang, Ying Yu, Yun Fan, Hui Li

Thymic epithelial tumors (TETs) are rare neoplasms of the anterior mediastinum that arise from thymic epithelial cells. Although surgery is the preferred treatment for resectable TETs, the options for unresectable or recurrent advanced-stage TETs are limited beyond platinum-based chemotherapy. The evolving landscape of TET treatments is marked by significant advancements in targeted therapies and immunotherapies, particularly with anti-angiogenic agents and immune checkpoint inhibitors (ICIs). While monotherapies demonstrated certain efficacy, the development of combination strategies is vital for improving patient outcomes. This review consolidates progress in anti-angiogenic therapies and ICIs, emphasizing the evolution of combination therapies of TETs. Furtherly, we particularly discuss new first-line strategies based on these advancements and emphasizes exploring novel treatments like antibody-drug conjugates, immunomodulatory drugs and cytokine-based agents for TETs. Mechanistically, the molecular features of TETs integrated with clinical diagnosis and targeted therapy, and immunophenotyping of TETs along with its impact on the efficacy and safety of immunotherapy are discussed. Thus, this review systemizes the development in the treatment landscape of TETs, integrating the corresponding molecular and immune mechanisms, aiming to provide new references for the treatment of TETs.

胸腺上皮肿瘤(TET)是前纵隔的罕见肿瘤,由胸腺上皮细胞产生。虽然手术是可切除 TET 的首选治疗方法,但对于无法切除或复发的晚期 TET,除了铂类化疗外,其他治疗方法都很有限。靶向疗法和免疫疗法,尤其是抗血管生成药物和免疫检查点抑制剂(ICIs)的重大进展标志着 TET 治疗的不断发展。虽然单一疗法具有一定疗效,但联合疗法的开发对改善患者预后至关重要。本综述总结了抗血管生成疗法和 ICIs 的进展,强调了 TETs 联合疗法的演变。此外,我们还特别讨论了基于这些进展的新一线治疗策略,并强调探索用于 TETs 的抗体药物共轭物、免疫调节药物和细胞因子类药物等新型治疗方法。从机理上讲,TETs 的分子特征与临床诊断和靶向治疗相结合,TETs 的免疫分型及其对免疫疗法疗效和安全性的影响也在讨论之列。因此,这篇综述系统地介绍了TETs治疗的发展情况,整合了相应的分子和免疫机制,旨在为TETs的治疗提供新的参考。
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