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Targeting the Hippo pathway in cancer: kidney toxicity as a class effect of TEAD inhibitors? 以癌症中的希波通路为靶点:肾毒性是 TEAD 抑制剂的一类效应?
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-11-08 DOI: 10.1016/j.trecan.2024.10.004
Sayantanee Paul, Jessica Sims, Trang Pham, Anwesha Dey

The Hippo pathway has emerged as a critical player in both cancers and targeted therapy resistance. Recent drug discovery efforts have led to the development of TEAD inhibitors, several of which have already progressed to the clinic. To truly leverage their potential as anticancer therapeutics, safety considerations, particularly in regard to the kidney, warrant additional investigation. This review explores the Hippo pathway's role in cancers, its therapeutic potential, role in kidney development, and the need to evaluate the best strategies to translate its clinical application for long-term patient benefit.

Hippo 通路已成为癌症和靶向治疗耐药性的关键因素。最近的药物发现工作已开发出 TEAD 抑制剂,其中几种已进入临床。要真正发挥其作为抗癌疗法的潜力,还需要对其安全性,尤其是对肾脏的安全性进行更多的研究。本综述探讨了希波通路在癌症中的作用、其治疗潜力、在肾脏发育中的作用,以及评估将其转化为临床应用以造福患者的最佳策略的必要性。
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引用次数: 0
Metabolic landscape of disseminated cancer dormancy. 扩散性癌症休眠的代谢景观
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-11-06 DOI: 10.1016/j.trecan.2024.10.005
Stanislav Drapela, Bruna M Garcia, Ana P Gomes, Ana Luísa Correia

Cancer dormancy is a phenomenon defined by the entry of cancer cells into a reversible quiescent, nonproliferative state, and represents an essential part of the metastatic cascade responsible for cancer recurrence and mortality. Emerging evidence suggests that metabolic reprogramming plays a pivotal role in enabling entry, maintenance, and exit from dormancy in the face of the different environments of the metastatic cascade. Here, we review the current literature to understand the dynamics of metabolism during dormancy, highlighting its fine-tuning by the host micro- and macroenvironment, and put forward the importance of identifying metabolic vulnerabilities of the dormant state as therapeutic targets to eradicate recurrent disease.

癌症休眠是指癌细胞进入一种可逆的静止、非增殖状态,是导致癌症复发和死亡的转移级联的重要组成部分。新的证据表明,面对转移级联的不同环境,代谢重编程在使癌细胞进入、维持和脱离休眠状态方面发挥着关键作用。在此,我们回顾了目前的文献,以了解休眠期新陈代谢的动态,强调宿主微环境和大环境对新陈代谢的微调,并提出了将休眠状态下的新陈代谢漏洞确定为根除复发疾病的治疗靶点的重要性。
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引用次数: 0
Epigenetic control of immunoevasion in cancer stem cells. 癌症干细胞免疫逃逸的表观遗传学控制。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-11-01 Epub Date: 2024-09-06 DOI: 10.1016/j.trecan.2024.08.004
Claudia Galassi, Manel Esteller, Ilio Vitale, Lorenzo Galluzzi

Cancer stem cells (CSCs) are a poorly differentiated population of malignant cells that (at least in some neoplasms) is responsible for tumor progression, resistance to therapy, and disease relapse. According to a widely accepted model, all stages of cancer progression involve the ability of neoplastic cells to evade recognition or elimination by the host immune system. In line with this notion, CSCs are not only able to cope with environmental and therapy-elicited stress better than their more differentiated counterparts but also appear to better evade tumor-targeting immune responses. We summarize epigenetic modifications of DNA and histones through which CSCs evade immune recognition or elimination, and propose that such alterations constitute promising therapeutic targets to increase the sensitivity of some malignancies to immunotherapy.

癌症干细胞(CSCs)是一种分化不良的恶性细胞群,(至少在某些肿瘤中)是肿瘤进展、抗药性和疾病复发的罪魁祸首。根据一种广为接受的模式,癌症进展的所有阶段都涉及肿瘤细胞逃避宿主免疫系统识别或清除的能力。根据这一概念,癌细胞干细胞不仅能比其分化程度较高的同类细胞更好地应对环境和治疗引发的压力,而且似乎还能更好地逃避肿瘤靶向免疫反应。我们总结了DNA和组蛋白的表观遗传学修饰,通过这些修饰,CSCs可以逃避免疫识别或消灭,并提出这种改变是很有希望的治疗靶点,可以提高一些恶性肿瘤对免疫疗法的敏感性。
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引用次数: 0
Mechanisms governing lineage plasticity and metabolic reprogramming in cancer. 癌症的血统可塑性和代谢重编程机制。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-11-01 Epub Date: 2024-08-31 DOI: 10.1016/j.trecan.2024.08.001
Lillian M Perez, Smrruthi V Venugopal, Anna St Martin, Stephen J Freedland, Dolores Di Vizio, Michael R Freeman

Dynamic alterations in cellular phenotypes during cancer progression are attributed to a phenomenon known as 'lineage plasticity'. This process is associated with therapeutic resistance and involves concurrent shifts in metabolic states that facilitate adaptation to various stressors inherent in malignant growth. Certain metabolites also serve as synthetic reservoirs for chromatin modification, thus linking metabolic states with epigenetic regulation. There remains a critical need to understand the mechanisms that converge on lineage plasticity and metabolic reprogramming to prevent the emergence of lethal disease. This review attempts to offer an overview of our current understanding of the interplay between metabolic reprogramming and lineage plasticity in the context of cancer, highlighting the intersecting drivers of cancer hallmarks, with an emphasis on solid tumors.

癌症发展过程中细胞表型的动态变化归因于一种被称为 "品系可塑性 "的现象。这一过程与治疗耐药性有关,涉及代谢状态的同时转变,这种转变有助于适应恶性肿瘤生长过程中固有的各种压力。某些代谢物还可作为染色质修饰的合成库,从而将代谢状态与表观遗传调控联系起来。目前,我们仍然亟需弄清血统可塑性和代谢重编程的趋同机制,以防止致命疾病的出现。本综述试图概述我们目前对癌症背景下代谢重编程和品系可塑性之间相互作用的理解,强调癌症特征的交叉驱动因素,重点是实体瘤。
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引用次数: 0
Trends in cancer imaging. 癌症成像趋势。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-11-01 Epub Date: 2024-09-04 DOI: 10.1016/j.trecan.2024.08.006
Xinyuan Zhou, Binyu Shi, Gang Huang, Jianjun Liu, Weijun Wei

Molecular imaging of cancer is a collaborative endeavor, uniting scientists and physicians from diverse fields. Such collaboration is actively developing and translating cutting-edge molecular imaging approaches to enhance the diagnostic landscape of human malignancies. The advent of positron emission tomography (PET) and PET imaging tracers has realized non-invasive target annotation and tumor characterization at the molecular level. In surgical procedures, novel imaging techniques, such as fluorescence or Cherenkov luminescence, help identify tumors and enhance surgical precision. Simultaneously, progress in imaging equipment, innovative algorithms, and artificial intelligence has opened avenues for next-generation cancer screening and imaging, augmenting the efficiency and accuracy of cancer diagnosis. In this review, we provide a panorama of molecular cancer imaging and ongoing developments in the field.

癌症分子成像是一项合作性工作,它将来自不同领域的科学家和医生团结在一起。这种合作正在积极开发和转化最前沿的分子成像方法,以改善人类恶性肿瘤的诊断状况。正电子发射断层扫描(PET)和 PET 成像示踪剂的出现实现了分子水平的无创靶标标注和肿瘤特征描述。在外科手术中,荧光或切伦科夫发光等新型成像技术有助于识别肿瘤并提高手术精确度。与此同时,成像设备、创新算法和人工智能的进步为下一代癌症筛查和成像开辟了道路,提高了癌症诊断的效率和准确性。在这篇综述中,我们将介绍癌症分子成像的全景以及该领域的持续发展。
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引用次数: 0
Prognostic value of atypical B cells in breast cancer. 乳腺癌非典型 B 细胞的预后价值。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-11-01 Epub Date: 2024-10-01 DOI: 10.1016/j.trecan.2024.09.009
Esmeralda García-Torralba, Lorenzo Galluzzi, Aitziber Buqué

The impact of tumor-infiltrating B cells on breast cancer (BRCA) outcomes remains poorly understood. Recent findings from Yang et al. identify an atypical, clonally expanded population of activated Fc receptor-like 4 (FCRL4)+ B cells that is associated with improved overall survival in patients affected by various tumor types, including BRCA.

人们对肿瘤浸润性 B 细胞对乳腺癌(BRCA)预后的影响仍然知之甚少。Yang等人的最新研究发现,活化的Fc受体样4(FCRL4)+B细胞是一种非典型、克隆性扩增的细胞群,它与包括BRCA在内的各种肿瘤患者总生存率的提高有关。
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引用次数: 0
Accessing the vasculature in cancer: revising an old hallmark. 进入癌症血管:重新审视古老的标志。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-11-01 Epub Date: 2024-10-02 DOI: 10.1016/j.trecan.2024.08.003
Adrian L Harris, David J Kerr, Francesco Pezzella, Domenico Ribatti

The classic cancer hallmark, inducing angiogenesis, was born out of the long-held notion that tumours could grow only if new vessels were formed. The attempts, based on this premise, to therapeutically restrain angiogenesis in hopes of controlling tumour growth have been less effective than expected. This is partly because primary and metastatic tumours can grow without angiogenesis. The discovery of nonangiogenic cancers and the mechanisms they use to exploit normal vessels, called 'vessel co-option,' has opened a new field in cancer biology. Consequently, the cancer hallmark, 'inducing angiogenesis,' has been modified to 'inducing or accessing vasculature.'

诱导血管生成是典型的癌症标志,它的诞生源于人们长期以来的一种观念,即只有形成新的血管,肿瘤才能生长。基于这一前提,人们试图通过治疗手段抑制血管生成以控制肿瘤生长,但效果不如预期。部分原因是原发性和转移性肿瘤可以在没有血管生成的情况下生长。非血管生成癌症及其利用正常血管的机制(称为 "血管共用")的发现为癌症生物学开辟了一个新领域。因此,癌症的标志 "诱导血管生成 "已被修改为 "诱导或利用血管"。
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引用次数: 0
Time to heal: inhibiting fibrosis prevents glioblastoma recurrence. 愈合时间:抑制纤维化可预防胶质母细胞瘤复发。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-11-01 Epub Date: 2024-10-02 DOI: 10.1016/j.trecan.2024.09.008
Dhanashree Mundhe, Neta Erez

New findings by Watson et al. demonstrate that therapy-induced inflammation and fibrosis potentiate glioblastoma recurrence. Post-treatment fibrotic niches shielded surviving tumor cells from immune surveillance, supported their persistence in a dormant state, and enabled rebound growth. Timely inhibition of inflammation and scarring attenuated recurrence, encouraging the use of new combinatorial approaches in glioblastoma therapy.

Watson等人的新发现表明,治疗诱导的炎症和纤维化会加剧胶质母细胞瘤的复发。治疗后的纤维化龛使存活的肿瘤细胞免受免疫监视,支持其持续处于休眠状态,并使其反弹生长。及时抑制炎症和瘢痕可减轻复发,鼓励在胶质母细胞瘤治疗中使用新的组合方法。
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引用次数: 0
Transcriptional regulation of hypoxic cancer cell metabolism and artificial intelligence. 缺氧癌细胞新陈代谢的转录调控与人工智能。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-10-30 DOI: 10.1016/j.trecan.2024.10.003
Luana Schito, Sergio Rey-Keim

Gene expression regulation in hypoxic tumor microenvironments is mediated by O2 responsive transcription factors (O2R-TFs), fine-tuning cancer cell metabolic demand for O2 according to its availability. Here, we discuss key O2R-TFs and emerging artificial intelligence (AI)-based applications suitable for the interrogation of O2R-TF relationships specifying cancer cell metabolic adaptations to hypoxia.

缺氧肿瘤微环境中的基因表达调控是由氧气反应性转录因子(O2R-TFs)介导的,根据氧气的可用性微调癌细胞对氧气的代谢需求。在此,我们将讨论关键的 O2R-TFs 和基于人工智能 (AI) 的新兴应用,这些应用适用于研究 O2R-TF 关系,从而确定癌细胞对缺氧的代谢适应性。
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引用次数: 0
The UPRising connection between endoplasmic reticulum stress and the tumor microenvironment. 内质网应激与肿瘤微环境之间的联系日益突出。
IF 14.3 1区 医学 Q1 ONCOLOGY Pub Date : 2024-10-29 DOI: 10.1016/j.trecan.2024.09.011
Hery Urra, Raúl Aravena, Lucas González-Johnson, Claudio Hetz

The tumor microenvironment (TME) represents a dynamic network of cancer cells, stromal cells, immune mediators, and extracellular matrix components, crucial for cancer progression. Stress conditions such as oncogene activation, nutrient deprivation, and hypoxia disrupt the endoplasmic reticulum (ER), activating the unfolded protein response (UPR), the main adaptive mechanism to restore ER function. The UPR regulates cancer progression by engaging cell-autonomous and cell-non-autonomous mechanisms, reprogramming the stroma and promoting immune evasion, angiogenesis, and invasion. This review explores the role of UPR beyond cancer cells, focusing on how ER stress signaling reshapes the TME, supporting tumor growth. The therapeutic potential of targeting the UPR is also discussed.

肿瘤微环境(TME)是由癌细胞、基质细胞、免疫介质和细胞外基质成分组成的动态网络,对癌症的进展至关重要。癌基因激活、营养匮乏和缺氧等应激条件会破坏内质网(ER),激活未折叠蛋白反应(UPR),这是恢复ER功能的主要适应机制。UPR 通过调动细胞自主和细胞非自主机制、重塑基质以及促进免疫逃避、血管生成和侵袭来调控癌症进展。本综述探讨了 UPR 在癌细胞之外的作用,重点关注 ER 应激信号如何重塑 TME,从而支持肿瘤生长。此外,还讨论了针对 UPR 的治疗潜力。
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Trends in cancer
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