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The origin of novel traits in cancer. 癌症新性状的起源
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-10-01 Epub Date: 2024-08-06 DOI: 10.1016/j.trecan.2024.07.005
Steven A Frank, Itai Yanai

The traditional view of cancer emphasizes a genes-first process. Novel cancer traits arise by genetic mutations that spread to drive phenotypic change. However, recent data support a phenotypes-first process in which nonheritable cellular variability creates novel traits that later become heritably stabilized by genetic and epigenetic changes. Single-cell measurements reinforce the idea that phenotypes lead genotypes, showing how cancer evolution follows normal developmental plasticity and creates novel traits by recombining parts of different cellular developmental programs. In parallel, studies in evolutionary biology also support a phenotypes-first process driven by developmental plasticity and developmental recombination. These advances in cancer research and evolutionary biology mutually reinforce a revolution in our understanding of how cells and organisms evolve novel traits in response to environmental challenges.

传统的癌症观点强调基因优先的过程。新的癌症特征是由基因突变产生的,基因突变的扩散推动了表型的改变。然而,最近的数据支持表型先行的过程,在这一过程中,不可遗传的细胞变异性产生了新的性状,这些性状随后通过遗传和表观遗传学变化而变得遗传稳定。单细胞测量强化了表型引导基因型的观点,显示了癌症进化如何遵循正常的发育可塑性,并通过重组不同细胞发育程序的部分内容来创造新的性状。与此同时,进化生物学研究也支持由发育可塑性和发育重组驱动的表型优先过程。癌症研究和进化生物学的这些进展相互促进,使我们对细胞和生物体如何进化出新的性状以应对环境挑战的理解发生了革命性的变化。
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引用次数: 0
Bispecific antibodies: advancing precision oncology. 双特异性抗体:推动精准肿瘤学的发展。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-10-01 Epub Date: 2024-08-30 DOI: 10.1016/j.trecan.2024.07.002
Mercedes Herrera, Giulia Pretelli, Jayesh Desai, Elena Garralda, Lillian L Siu, Thiago M Steiner, Lewis Au

Bispecific antibodies (bsAbs) are engineered molecules designed to target two different epitopes or antigens. The mechanism of action is determined by the bsAb molecular targets and structure (or format), which can be manipulated to create variable and novel functionalities, including linking immune cells with tumor cells, or dual signaling pathway blockade. Several bsAbs have already changed the treatment landscape of hematological malignancies and select solid cancers. However, the mechanisms of resistance to these agents are understudied and the management of toxicities remains challenging. Herein, we review the principles in bsAb engineering, current understanding of mechanisms of action and resistance, data for clinical application, and provide a perspective on ongoing challenges and future developments in this field.

双特异性抗体(bsAbs)是针对两种不同表位或抗原设计的工程分子。其作用机制由 bsAb 分子靶点和结构(或格式)决定,可通过对其进行操作创造出各种新功能,包括连接免疫细胞与肿瘤细胞或阻断双重信号通路。一些 bsAbs 已经改变了血液恶性肿瘤和部分实体瘤的治疗格局。然而,人们对这些药物的抗药性机制研究不足,对毒性的处理仍然充满挑战。在此,我们回顾了 bsAb 工程学的原理、目前对作用机制和耐药性的理解、临床应用数据,并展望了这一领域目前面临的挑战和未来的发展。
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引用次数: 0
CD4+ T cells in antitumor immunity. 抗肿瘤免疫中的 CD4+ T 细胞。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-10-01 Epub Date: 2024-09-05 DOI: 10.1016/j.trecan.2024.07.009
Elena Montauti, David Y Oh, Lawrence Fong

Advances in cancer immunotherapy have transformed cancer care and realized unprecedented responses in many patients. The growing arsenal of novel therapeutics - including immune checkpoint inhibition (ICI), adoptive T cell therapies (ACTs), and cancer vaccines - reflects the success of cancer immunotherapy. The therapeutic benefits of these treatment modalities are generally attributed to the enhanced quantity and quality of antitumor CD8+ T cell responses. Nevertheless, CD4+ T cells are now recognized to play key roles in both the priming and effector phases of the antitumor immune response. In addition to providing T cell help through co-stimulation and cytokine production, CD4+ T cells can also possess cytotoxicity either directly on MHC class II-expressing tumor cells or to other cells within the tumor microenvironment (TME). The presence of specific populations of CD4+ T cells, and their intrinsic plasticity, within the TME can represent an important determinant of clinical response to immune checkpoint inhibitors, vaccines, and chimeric antigen receptor (CAR) T cell therapies. Understanding how the antitumor functions of specific CD4+ T cell types are induced while limiting their protumorigenic attributes will enable more successful immunotherapies.

癌症免疫疗法的进步改变了癌症治疗,使许多患者获得了前所未有的治疗效果。包括免疫检查点抑制疗法(ICI)、收养 T 细胞疗法(ACTs)和癌症疫苗在内的新型疗法不断增加,反映了癌症免疫疗法的成功。这些治疗方法的疗效通常归功于抗肿瘤 CD8+ T 细胞应答数量和质量的提高。然而,现在人们认识到,CD4+ T 细胞在抗肿瘤免疫反应的起始阶段和效应阶段都发挥着关键作用。除了通过协同刺激和产生细胞因子为 T 细胞提供帮助外,CD4+ T 细胞还能直接对 MHC II 类表达的肿瘤细胞或肿瘤微环境(TME)中的其他细胞产生细胞毒性。TME 中特定 CD4+ T 细胞群的存在及其内在可塑性是决定免疫检查点抑制剂、疫苗和嵌合抗原受体(CAR)T 细胞疗法临床反应的重要因素。了解如何诱导特定 CD4+ T 细胞类型的抗肿瘤功能,同时限制它们的原发肿瘤属性,将使免疫疗法更加成功。
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引用次数: 0
EZHIP's role in diffuse midline glioma: echoes of oncohistones? EZHIP 在弥漫性中线胶质瘤中的作用:与癌基因的呼应?
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-09-28 DOI: 10.1016/j.trecan.2024.09.002
Afraah Cassim, Matthew D Dun, David Gallego-Ortega, Fatima Valdes-Mora

The enhancer of zeste inhibitory protein (EZHIP) is typically expressed during germ cell development and has been classified as a cancer-testis antigen (CTA) in various cancers. In 2020, 4% of diffuse midline gliomas (DMGs) were shown to aberrantly express EZHIP, mirroring the DMG hallmark histone H3 K27M (H3K27M) oncohistone mutation. Similar to H3K27M, EZHIP is a negative regulator of polycomb repressive complex 2 (PRC2), leading to global epigenomic remodeling. In this opinion, we explore the similarities and disparities between H3K27M- and EZHIP-DMGs with a focus on their shared functional hallmark of PRC2 inhibition, their genetic and epigenomic landscapes, plausible differences in the cell of origin, and therapeutic avenues. Upcoming research on EZHIP will help better understand its role in gliomagenesis and DMG therapy.

泽斯特增强子抑制蛋白(EZHIP)通常在生殖细胞发育过程中表达,在各种癌症中被归类为癌睾抗原(CTA)。2020 年,4% 的弥漫中线胶质瘤(DMGs)被证明异常表达 EZHIP,这与 DMG 标志性组蛋白 H3 K27M(H3K27M)同源突变如出一辙。与 H3K27M 相似,EZHIP 也是多聚酶抑制复合体 2(PRC2)的负调控因子,可导致全球表观基因组重塑。在这篇论文中,我们探讨了 H3K27M- 和 EZHIP-DMGs 的异同,重点是它们共同的功能特征:PRC2 抑制、它们的遗传和表观基因组图谱、起源细胞中可能存在的差异以及治疗途径。即将开展的有关EZHIP的研究将有助于更好地了解它在胶质瘤发生和DMG治疗中的作用。
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引用次数: 0
Cancer researchers as storytellers for the lay public. 癌症研究人员为普通公众讲故事。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-09-27 DOI: 10.1016/j.trecan.2024.09.004
William G Nelson

Cancer researchers tend to be well-versed in communicating research and research results to scientific audiences. To maintain momentum and progress against cancer, they must acquire and nurture skills allowing for better engagement with the lay public.

癌症研究人员往往精通向科学受众传播研究和研究成果。为了保持抗击癌症的势头和进展,他们必须掌握和培养与非专业公众进行更好交流的技能。
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引用次数: 0
Crosstalk of T cells within the ovarian cancer microenvironment. 卵巢癌微环境中 T 细胞的相互影响。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-09-27 DOI: 10.1016/j.trecan.2024.09.001
Bovannak S Chap, Nicolas Rayroux, Alizée J Grimm, Eleonora Ghisoni, Denarda Dangaj Laniti

Ovarian cancer (OC) represents ecosystems of highly diverse tumor microenvironments (TMEs). The presence of tumor-infiltrating lymphocytes (TILs) is linked to enhanced immune responses and long-term survival. In this review we present emerging evidence suggesting that cellular crosstalk tightly regulates the distribution of TILs within the TME, underscoring the need to better understand key cellular networks that promote or impede T cell infiltration in OC. We also capture the emergent methodologies and computational techniques that enable the dissection of cell-cell crosstalk. Finally, we present innovative ex vivo TME models that can be leveraged to map and perturb cellular communications to enhance T cell infiltration and immune reactivity.

卵巢癌(OC)代表着高度多样化的肿瘤微环境(TME)生态系统。肿瘤浸润淋巴细胞(TILs)的存在与增强的免疫反应和长期生存有关。在这篇综述中,我们介绍了新出现的证据,这些证据表明细胞间的串联密切调节着 TILs 在 TME 中的分布,强调了更好地了解促进或阻碍 T 细胞浸润 OC 的关键细胞网络的必要性。我们还捕捉了新出现的方法和计算技术,这些方法和技术有助于剖析细胞-细胞串联。最后,我们介绍了创新的体外 TME 模型,这些模型可用于绘制和扰乱细胞通讯,以增强 T 细胞浸润和免疫反应性。
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引用次数: 0
Malignant glioma remodeling of neuronal circuits: therapeutic opportunities and repurposing of antiepileptic drugs. 恶性胶质瘤重塑神经元回路:治疗机会和抗癫痫药物的再利用。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-09-25 DOI: 10.1016/j.trecan.2024.09.003
Cesar Nava Gonzales, Mikias B Negussie, Saritha Krishna, Vardhaan S Ambati, Shawn L Hervey-Jumper

Tumor-associated epilepsy is the most common presenting symptom in patients diagnosed with diffuse gliomas. Recent evidence illustrates the requirement of synaptic activity to drive glioma proliferation and invasion. Class 1, 2, and 3 evidence is limited regarding the use of antiepileptic drugs (AEDs) as antitumor therapy in combination with chemotherapy. Furthermore, no central mechanism has emerged as the most targetable. The optimal timing of AED regimen remains unknown. Targeting aberrant neuronal activity is a promising avenue for glioma treatment. Clinical biomarkers may aid in identifying patients most likely to benefit from AEDs. Quality evidence is needed to guide treatment decisions.

肿瘤相关性癫痫是弥漫性胶质瘤患者最常见的症状。最近的证据表明,胶质瘤的增殖和侵袭需要突触活动的驱动。关于使用抗癫痫药物(AEDs)与化疗联合进行抗肿瘤治疗,1 级、2 级和 3 级证据十分有限。此外,还没有发现最有针对性的中心机制。抗癫痫药物治疗的最佳时机仍然未知。以异常神经元活动为靶点是治疗胶质瘤的一个前景广阔的途径。临床生物标志物可能有助于确定最有可能从AEDs中获益的患者。需要高质量的证据来指导治疗决策。
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引用次数: 0
Immunomodulation by endothelial cells: prospects for cancer therapy 内皮细胞的免疫调节作用:癌症治疗的前景
IF 18.4 1区 医学 Q1 ONCOLOGY Pub Date : 2024-09-16 DOI: 10.1016/j.trecan.2024.08.002
Halima Alnaqbi, Lisa M. Becker, Mira Mousa, Fatima Alshamsi, Sarah K. Azzam, Besa Emini Veseli, Lauren A. Hymel, Khalood Alhosani, Marwa Alhusain, Massimiliano Mazzone, Habiba Alsafar, Peter Carmeliet

Growing evidence highlights the importance of tumor endothelial cells (TECs) in the tumor microenvironment (TME) for promoting tumor growth and evading immune responses. Immunomodulatory endothelial cells (IMECs) represent a distinct plastic phenotype of ECs that exerts the ability to modulate immunity in health and disease. This review discusses our current understanding of IMECs in cancer biology, scrutinizing insights from single-cell reports to compare their characteristics and function dynamics across diverse tumor types, conditions, and species. We investigate possible implications of exploiting IMECs in the context of cancer treatment, particularly examining their influence on the efficacy of existing therapies and the potential to leverage them as targets in optimizing immunotherapeutic strategies.

越来越多的证据表明,肿瘤微环境(TME)中的肿瘤内皮细胞(TECs)对促进肿瘤生长和逃避免疫反应非常重要。免疫调节内皮细胞(IMECs)代表了一种独特的可塑性内皮细胞表型,在健康和疾病中发挥着调节免疫的能力。本综述讨论了我们目前对癌症生物学中 IMECs 的理解,仔细研究了单细胞报告的见解,比较了它们在不同肿瘤类型、条件和物种中的特征和功能动态。我们探讨了在癌症治疗中利用 IMECs 可能产生的影响,特别是研究了它们对现有疗法疗效的影响,以及将它们作为优化免疫治疗策略靶点的潜力。
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引用次数: 0
Metabolism and epigenetics: drivers of tumor cell plasticity and treatment outcomes 代谢和表观遗传学:肿瘤细胞可塑性和治疗效果的驱动因素
IF 18.4 1区 医学 Q1 ONCOLOGY Pub Date : 2024-09-14 DOI: 10.1016/j.trecan.2024.08.005
Benjamin N. Gantner, Flavio R. Palma, Madhura R. Pandkar, Marcelo J. Sakiyama, Daniel Arango, Gina M. DeNicola, Ana P. Gomes, Marcelo G. Bonini

Emerging evidence indicates that metabolism not only is a source of energy and biomaterials for cell division but also acts as a driver of cancer cell plasticity and treatment resistance. This is because metabolic changes lead to remodeling of chromatin and reprogramming of gene expression patterns, furthering tumor cell phenotypic transitions. Therefore, the crosstalk between metabolism and epigenetics seems to hold immense potential for the discovery of novel therapeutic targets for various aggressive tumors. Here, we highlight recent discoveries supporting the concept that the cooperation between metabolism and epigenetics enables cancer to overcome mounting treatment-induced pressures. We discuss how specific metabolites contribute to cancer cell resilience and provide perspective on how simultaneously targeting these key forces could produce synergistic therapeutic effects to improve treatment outcomes.

新的证据表明,新陈代谢不仅是细胞分裂的能量和生物材料来源,而且还是癌细胞可塑性和耐药性的驱动因素。这是因为新陈代谢的变化会导致染色质的重塑和基因表达模式的重编程,进一步推动肿瘤细胞表型的转变。因此,新陈代谢与表观遗传学之间的相互影响似乎蕴含着发现各种侵袭性肿瘤的新型治疗靶点的巨大潜力。在此,我们重点介绍最近的发现,这些发现支持了这样一个概念,即代谢和表观遗传学之间的合作使癌症能够克服日益增加的治疗压力。我们讨论了特定的代谢物如何促进癌细胞的恢复能力,并透视了同时针对这些关键力量如何产生协同治疗效果以改善治疗效果。
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引用次数: 0
Scaling data toward pan-cancer foundation models 扩大数据规模,建立泛癌症基础模型
IF 18.4 1区 医学 Q1 ONCOLOGY Pub Date : 2024-09-11 DOI: 10.1016/j.trecan.2024.08.008
Nadieh Khalili, Francesco Ciompi

Recent advances in artificial intelligence (AI) have revolutionized computational pathology (CPath), particularly through deep learning (DL) and neural networks (NNs). In a recent study, Vorontsov et al. introduced Virchow, a new foundation model (FM) for CPath, which has shown promising results in cancer detection and biomarker prediction.

人工智能(AI)的最新进展给计算病理学(CPath)带来了革命性的变化,特别是通过深度学习(DL)和神经网络(NN)。在最近的一项研究中,Vorontsov 等人为 CPath 引入了一种新的基础模型 (FM)--Virchow,该模型在癌症检测和生物标记预测方面取得了令人鼓舞的成果。
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引用次数: 0
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Trends in cancer
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