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Cellular plasticity and non-small cell lung cancer: role of T and NK cell immune evasion and acquisition of resistance to immunotherapies. 细胞可塑性与非小细胞肺癌:T 细胞和 NK 细胞免疫逃避和获得免疫疗法抗药性的作用。
IF 7.7 2区 医学 Q1 ONCOLOGY Pub Date : 2025-01-25 DOI: 10.1007/s10555-025-10244-8
Sarra Mestiri, Ana Sami, Naresh Sah, Dina Moustafa Abo El-Ella, Sabiha Khatoon, Khadija Shafique, Afsheen Raza, Darin Mansor Mathkor, Shafiul Haque

Lung cancer is a leading global cause of mortality, with non-small cell lung cancer (NSCLC) accounting for a significant portion of cases. Immune checkpoint inhibitors (ICIs) have transformed NSCLC treatment; however, many patients remain unresponsive. ICI resistance in NSCLC and its association with cellular plasticity, epithelial-mesenchymal transition (EMT), enhanced adaptability, invasiveness, and resistance is largely influenced by epigenetic changes, signaling pathways, tumor microenvironment, and associated immune cells, fibroblasts, and cytokines. Immunosuppressive cells, including M2 tumor-associated macrophages, myeloid-derived suppressor cells, and regulatory T cells, contribute to resistance by suppressing the immune response. This cellular plasticity is influenced when B cells, natural killer cells, and T cells are exhausted or inhibited by components of the tumor microenvironment. Conversely, diverse T cell, NK cell, and B cell subsets hold potential as predictive response markers particularly cytotoxic CD8+ T cells, effector memory T cells, activated T cells, tumor infiltrated NK cells, tertiary lymphoid structures, etc. influence treatment response. Identifying specific gene expressions and immunophenotypes within T cells may offer insights into early clinical responses to immunotherapy. ICI resistance in NSCLC is a multifaceted process shaped by tumor plasticity, the complex tumor microenvironment, and dynamic immune cell changes. Comprehensive analysis of these factors may lead to the identification of novel biomarkers and combination therapies to enhance ICI efficacy in NSCLC treatment.

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引用次数: 0
The diversity of natural killer cell functional and phenotypic states in cancer.
IF 7.7 2区 医学 Q1 ONCOLOGY Pub Date : 2025-01-24 DOI: 10.1007/s10555-025-10242-w
Kumar Rishabh, Sandro Matosevic

The role of natural killer (NK) cells as immune effectors is well established, as is their utility as immunotherapeutic agents against various cancers. However, NK cells' anti-cancer roles are suppressed in cancer patients by various immunomodulatory mechanisms which alter these cells' identity, function, and potential for immunosurveillance. This manifests in abnormal NK cell responses accompanied by changes in phenotypic or genotypic identity, giving rise to specific NK cell subsets that are either hypofunctional or, more broadly, defective in their responses. Anergy, senescence, and exhaustion are some of the terms that have been used to define and characterize these NK cell functional states. These responses vary not only with cancer type but also NK cell location within tissues. Collectively, these phenomena suggest a highly plastic nature of NK cell biology in tumors. In this review, we present and discuss a summary of these functionally distinct states and provide an overview of how NK cells behave at different locations within the context of cancer.

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引用次数: 0
Sympathetic nerve signaling rewires the tumor microenvironment: a shift in "microenvironmental-ity". 交感神经信号重塑肿瘤微环境:“微环境”的转变。
IF 7.7 2区 医学 Q1 ONCOLOGY Pub Date : 2025-01-20 DOI: 10.1007/s10555-025-10241-x
Ariana Sattler, Tetiana Korzun, Kasmira Gupta, Parham Diba, Natasha Kyprianou, Sebnem Ece Eksi

Nerve signaling within the tumor microenvironment (TME) plays a critical role in the initiation, progression, and metastasis of solid tumors. Due to their highly responsive behavior and activation upon injury and cancer onset, this review specifically focuses on how sympathetic nerves rewire the TME. Within tumors, sympathetic nerves closely interact with various TME components, and their combined signaling often shifts tumor-intrinsic physiology toward tumor-supportive phenotypes. In turn, the TME components, such as myeloid cells, lymphoid cells, extracellular matrix (ECM), endothelial cells, cancer associated fibroblasts (CAFs), and Schwann cells, secrete neurotrophic and axon guidance factors that influence both sympathetic outgrowth and tumor cell behavior, further exacerbating tumor progression and metastasis. Here, we review the current evidence on the multidirectional impacts of sympathetic nerves and both immune and non-immune TME components, the nature of these communication processes, and how exploring these interactions may inform future therapeutics to impair cancer progression and metastasis.

肿瘤微环境(tumor microenvironment, TME)内的神经信号在实体瘤的发生、发展和转移中起着至关重要的作用。由于交感神经在损伤和癌症发作时的高度反应行为和激活,本综述特别关注交感神经如何重新连接TME。在肿瘤中,交感神经与各种TME成分密切相互作用,它们的联合信号常常将肿瘤内在生理转向肿瘤支持表型。反过来,骨髓细胞、淋巴细胞、细胞外基质(ECM)、内皮细胞、癌症相关成纤维细胞(CAFs)和雪旺细胞等TME成分分泌神经营养和轴突引导因子,影响交感神经生长和肿瘤细胞行为,进一步加剧肿瘤进展和转移。在这里,我们回顾了目前关于交感神经和免疫和非免疫TME组分的多向影响的证据,这些通信过程的性质,以及如何探索这些相互作用可能为未来的治疗提供信息,以延缓癌症的进展和转移。
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引用次数: 0
Advancements in gene therapies targeting mutant KRAS in cancers. 靶向突变KRAS的癌症基因治疗进展。
IF 7.7 2区 医学 Q1 ONCOLOGY Pub Date : 2025-01-17 DOI: 10.1007/s10555-025-10243-9
Yuhang Wang, Thuy Anh Bui, Xinpu Yang, Gyorgy Hutvagner, Wei Deng

Mutations in the KRAS gene are well-known tumourigenic drivers of colorectal, pancreatic and lung cancers. Mechanistically, these mutations promote uncontrolled cell proliferation and alter the tumour microenvironment during early carcinoma stages. Given their critical carcinogenic functions, significant progress has been made in developing KRAS inhibitors for cancer treatment. However, clinical applications of these KRAS inhibitor compounds are limited to specific cancer types which carry the relevant KRAS mutations. Additionally, clinical findings have shown that these compounds can induce moderate to serious side effects. Therefore, new approaches have emerged focusing on the development of universal therapeutics capable of targeting a wider range of KRAS mutations, minimising toxicity and enhancing the therapeutic efficacy. This review aims to examine these therapeutic strategies in the context of cancer treatment. It firstly provides an overview of fundamental KRAS biology within the cell signalling landscape and how KRAS mutations are associated with cancer pathogenesis. Subsequently, it introduces the development of current KRAS inhibitors which target certain KRAS mutants in different types of cancer. It then explores the potential of gene therapy approaches, including siRNA, miRNA and CRISPR methodologies. Furthermore, it discusses the use of lipid-based nanocarriers to deliver gene cargos for targeting KRAS gene mutants. Finally, it provides the insights into the future prospects for combatting KRAS mutation-associated cancers.

KRAS基因突变是众所周知的结直肠癌、胰腺癌和肺癌的致瘤驱动因素。在机制上,这些突变促进不受控制的细胞增殖并改变早期癌症阶段的肿瘤微环境。鉴于其关键的致癌功能,开发用于癌症治疗的KRAS抑制剂取得了重大进展。然而,这些KRAS抑制剂化合物的临床应用仅限于携带相关KRAS突变的特定癌症类型。此外,临床研究结果表明,这些化合物可引起中度至严重的副作用。因此,新的方法已经出现,重点是开发能够靶向更广泛的KRAS突变的通用治疗方法,最小化毒性并提高治疗效果。这篇综述的目的是在癌症治疗的背景下检查这些治疗策略。它首先提供了基本的KRAS生物学在细胞信号传导景观和KRAS突变如何与癌症发病机制相关的概述。随后,介绍了目前针对不同类型癌症中某些KRAS突变体的KRAS抑制剂的发展。然后探索基因治疗方法的潜力,包括siRNA, miRNA和CRISPR方法。此外,它还讨论了使用基于脂质的纳米载体来递送靶向KRAS基因突变的基因货物。最后,它提供了对抗KRAS突变相关癌症的未来前景的见解。
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引用次数: 0
LGR5: An emerging therapeutic target for cancer metastasis and chemotherapy resistance. LGR5:肿瘤转移和化疗耐药的新靶点
IF 7.7 2区 医学 Q1 ONCOLOGY Pub Date : 2025-01-17 DOI: 10.1007/s10555-024-10239-x
Wanqi Wang, Noor A Lokman, Simon C Barry, Martin K Oehler, Carmela Ricciardelli

Cancer stem cells play an important role in tumor progression and chemotherapy resistance. Leucine-rich G repeat-containing protein-coupled receptor 5 (LGR5) has been identified as a cancer stem cell marker in several cancer types. LGR5 is involved in cancer development and progression via several pathways including WNT/β-catenin signaling pathway. LGR5 plays a role in tumor progression by promoting cancer cell migration, invasion, metastasis, and angiogenesis in many cancers including colorectal, brain, gastric, and ovarian cancer. This review summarises the current knowledge on the expression and functional role of LGR5 in cancers, the molecular mechanisms regulated by LGR5, and the relationship between LGR5 and chemotherapy resistance. The review also includes highlights potential strategies to inhibit LGR5 expression and function. The majority of functional studies have shown that LGR5 plays an important role in promoting cancer progression, metastasis and chemotherapy resistance however, in some contexts LGR5 can also activate tumor-suppressive pathways and LGR5 negative cells can also promote cancer progression. The review highlights that targeting LGR5 is a promising anti-cancer treatment but the functional effect of LGR5 on tumor cells is complex may be dependent on cancer type, tumor microenvironment and cross-talk with other molecules in the LGR5 signaling pathway.

肿瘤干细胞在肿瘤进展和化疗耐药中起着重要作用。富含亮氨酸的G重复序列蛋白偶联受体5 (LGR5)已被确定为几种癌症类型的癌症干细胞标志物。LGR5通过多种途径参与癌症的发生和进展,包括WNT/β-catenin信号通路。LGR5在包括结直肠癌、脑癌、胃癌和卵巢癌在内的许多癌症中,通过促进癌细胞迁移、侵袭、转移和血管生成,在肿瘤进展中发挥作用。本文就LGR5在肿瘤中的表达和功能作用、LGR5调控的分子机制以及LGR5与化疗耐药的关系等方面的研究进展进行综述。该综述还重点介绍了抑制LGR5表达和功能的潜在策略。大多数功能研究表明,LGR5在促进肿瘤进展、转移和化疗耐药中发挥重要作用,但在某些情况下,LGR5也可以激活肿瘤抑制通路,LGR5阴性细胞也可以促进癌症进展。综述强调,靶向LGR5是一种很有前景的抗癌治疗方法,但LGR5对肿瘤细胞的功能作用是复杂的,可能取决于肿瘤类型、肿瘤微环境以及LGR5信号通路中其他分子的串扰。
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引用次数: 0
The transcription factor FOXQ1 in cancer. 癌症中的转录因子FOXQ1。
IF 7.7 2区 医学 Q1 ONCOLOGY Pub Date : 2025-01-08 DOI: 10.1007/s10555-025-10240-y
Stefan Koch

FOXQ1 is a member of the large forkhead box (FOX) family of transcription factors that is involved in all aspects of mammalian development, physiology, and pathobiology. FOXQ1 has emerged as a major regulator of epithelial-to-mesenchymal transition and tumour metastasis in cancers, especially carcinomas of the digestive tract. Accordingly, FOXQ1 induction is recognised as an independent prognostic factor for worse overall survival in several types of cancer, including gastric and colorectal cancer. In this review article, I summarise new evidence on the role of FOXQ1 in cancer, with a focus on molecular mechanisms that control FOXQ1 levels and the regulation of FOXQ1 target genes. Unravelling the functions of FOXQ1 has the potential to facilitate the development of targeted treatments for metastatic cancers.

FOXQ1是大叉头盒(FOX)转录因子家族的一员,参与哺乳动物发育、生理和病理生物学的各个方面。FOXQ1已成为癌症,特别是消化道癌中上皮到间质转化和肿瘤转移的主要调节因子。因此,FOXQ1诱导被认为是几种癌症(包括胃癌和结直肠癌)总生存率较差的独立预后因素。在这篇综述文章中,我总结了关于FOXQ1在癌症中作用的新证据,重点是FOXQ1水平的分子控制机制和FOXQ1靶基因的调控。揭示FOXQ1的功能有可能促进转移性癌症靶向治疗的发展。
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引用次数: 0
Neuropeptide Y in cancer-biological functions and potential clinical implications. 神经肽Y在癌症生物学功能和潜在的临床意义。
IF 7.7 2区 医学 Q1 ONCOLOGY Pub Date : 2025-01-06 DOI: 10.1007/s10555-024-10237-z
Dawid Sigorski, Aleksandra Sejda, Nouran Abualsaud, Ewa Krawczyk, Ewa Izycka-Swieszewska, Joanna Kitlinska

Neuropeptide Y (NPY) is a sympathetic neurotransmitter widely distributed in the peripheral and central nervous system, affecting many physiological functions. Consequently, dysregulation of the NPY system contributes to numerous pathological disorders, including stress, obesity, and cancer. The pleiotropic functions of NPY in humans are mediated by G protein-coupled receptors (Y1R, Y2R, Y5R), which activate several signaling pathways and thereby regulate cell growth, differentiation, apoptosis, proliferation, angiogenesis, and metabolism. These activities of NPY are highly relevant to tumor biology and known hallmarks of cancer, including sustained proliferative potential, resisting cell death, angiogenesis, invasion, and metastases. In this comprehensive review, we describe the cellular functions of NPY and discuss its role in cancer pathobiology, as well as provide the current state of knowledge pertaining to NPY and its receptors in various cancer types. Moreover, we focus on potential clinical applications targeting the NPY system, such as its role as a prognostic and predictive factor, as well as its utility in cancer diagnostics, imaging, and treatment. Altogether, growing evidence supports the significant role of the NPY system in tumor pathobiology and implicates its potential therapeutic and diagnostic value in modern oncology.

神经肽Y (Neuropeptide Y, NPY)是一种广泛分布于外周和中枢神经系统的交感神经递质,影响多种生理功能。因此,NPY系统的失调会导致许多病理性疾病,包括压力、肥胖和癌症。人体NPY的多功能是通过G蛋白偶联受体(Y1R、Y2R、Y5R)介导的,这些受体激活多种信号通路,从而调节细胞生长、分化、凋亡、增殖、血管生成和代谢。NPY的这些活性与肿瘤生物学和已知的癌症特征高度相关,包括持续的增殖潜力、抵抗细胞死亡、血管生成、侵袭和转移。在这篇全面的综述中,我们描述了NPY的细胞功能,讨论了它在癌症病理生物学中的作用,并提供了有关NPY及其受体在各种癌症类型中的最新知识。此外,我们将重点关注针对NPY系统的潜在临床应用,例如其作为预后和预测因素的作用,以及其在癌症诊断,成像和治疗中的应用。总之,越来越多的证据支持NPY系统在肿瘤病理生物学中的重要作用,并暗示其在现代肿瘤学中的潜在治疗和诊断价值。
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引用次数: 0
Recapitulating the potential contribution of protein S-palmitoylation in cancer. 概述s -棕榈酰化蛋白在癌症中的潜在作用。
IF 7.7 2区 医学 Q1 ONCOLOGY Pub Date : 2024-12-27 DOI: 10.1007/s10555-024-10217-3
Suchi Chaturvedi, Avinash Sonawane

Protein S-palmitoylation is a reversible form of protein lipidation in which the formation of a thioester bond occurs between a cysteine (Cys) residue of a protein and a 16-carbon fatty acid chain. This modification is catalyzed by a family of palmitoyl acyl transferases, the DHHC enzymes, so called because of their Asp-His-His-Cys (DHHC) catalytic motif. Deregulation of DHHC enzymes has been linked to various diseases, including cancer and infections. Cancer, a major cause of global mortality, is characterized by features like uncontrolled cell growth, resistance to cell death, angiogenesis, invasion, and metastasis. Several of these processes are controlled by DHHC-mediated S-palmitoylation of oncogenes or tumor suppressors, including growth factor receptors (e.g., EGFR), kinases (e.g., AKT), and transcription factors (e.g., β-catenin). Dynamic regulation of S-palmitoylation is also governed by protein depalmitoylases. These enzymes balance the cycling of palmitoylation and regulate cellular signaling, cell growth, and its organization. Given the significance of S-palmitoylation in cancer, the DHHCs and protein depalmitoylases are promising targets for cancer therapy. Here we summarize the catalytic mechanisms of DHHC enzymes and depalmitoylases, their role in cancer progression and prevention, as well as the crosstalk of palmitoylation with other post-translational modifications. Additionally, we discuss the methods to detect S-palmitoylation, the limitations of available DHHC-targeting inhibitors, and ongoing research efforts to address these obstacles.

蛋白质s -棕榈酰化是一种可逆的蛋白质脂化形式,在蛋白质的半胱氨酸(Cys)残基和16碳脂肪酸链之间形成硫酯键。这种修饰是由棕榈酰酰基转移酶家族(DHHC酶)催化的,这样称呼是因为它们的Asp-His-His-Cys (DHHC)催化基序。解除DHHC酶的管制与各种疾病有关,包括癌症和感染。癌症是全球死亡的主要原因之一,其特点是细胞生长不受控制、细胞死亡抵抗、血管生成、侵袭和转移。这些过程中的一些是由dhhc介导的癌基因或肿瘤抑制因子的s -棕榈酰化控制的,包括生长因子受体(如EGFR)、激酶(如AKT)和转录因子(如β-catenin)。s -棕榈酰化的动态调节也由蛋白去棕榈酰化酶控制。这些酶平衡棕榈酰化循环,调节细胞信号,细胞生长及其组织。鉴于s -棕榈酰化在癌症中的重要意义,dhhc和蛋白去棕榈酰化酶是癌症治疗的有希望的靶点。本文综述了DHHC酶和去棕榈酰化酶的催化机制,它们在癌症进展和预防中的作用,以及棕榈酰化与其他翻译后修饰的相互作用。此外,我们讨论了检测s -棕榈酰化的方法,现有dhhc靶向抑制剂的局限性,以及正在进行的研究工作,以解决这些障碍。
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引用次数: 0
Homologous recombination deficiency (HRD) diagnostics: underlying mechanisms and new perspectives. 同源重组缺陷(HRD)诊断:潜在机制和新观点。
IF 7.7 2区 医学 Q1 ONCOLOGY Pub Date : 2024-12-26 DOI: 10.1007/s10555-024-10238-y
Andrey Kechin, Maksim Koryukov, Regina Mikheeva, Maksim Filipenko

Homologous recombination deficiency (HRD) is considered a universal and effective sign of a tumor's sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors. HRD diagnostics have undergone several stages of transformations: from detection of point mutations in HR-related genes and large regions with loss of heterozygosity detected using single-nucleotide polymorphism arrays to whole-genome signatures of single-nucleotide variants, large genomic rearrangements (LGRs), and copy number alterations. All these methods have their own advantages and limitations. HRD tests, based on signatures of LGRs and copy number alterations, show in hindsight that some progenitor cells have possessed HRD status but not the current state of the genome. The aim of this review was to compare different methods of HRD detection and mechanisms of formation of HRD-specific LGRs. In the last several years, new data appeared implying a crucial role of proteins BRCA1 and BRCA2 in the resolution of stalled replication forks that may be associated with at least some of LGRs observed in HRD-positive tumors. Reviewing current knowledge on these mechanisms, distributions of different LGR types, and limitations of sequencing technologies and algorithms of data analysis, we offer some new perspectives on HRD diagnostics. We hope that this review will help to accelerate the development of new diagnostic approaches in this important field of molecular oncology.

同源重组缺陷(HRD)被认为是肿瘤对聚adp核糖聚合酶(PARP)抑制剂敏感的普遍和有效的标志。HRD诊断经历了几个转变阶段:从检测hr相关基因的点突变和使用单核苷酸多态性阵列检测的大区域杂合性缺失,到单核苷酸变异的全基因组签名、大基因组重排(lgr)和拷贝数改变。这些方法都有各自的优点和局限性。基于lgr特征和拷贝数改变的HRD测试事后表明,一些祖细胞具有HRD状态,但不具有基因组的当前状态。这篇综述的目的是比较不同的HRD检测方法和HRD特异性lgr的形成机制。在过去的几年里,新的数据表明,BRCA1和BRCA2蛋白在解决停滞的复制分叉中起着至关重要的作用,这可能与至少一些在hrd阳性肿瘤中观察到的lgr有关。回顾目前关于这些机制的知识,不同LGR类型的分布,以及测序技术和数据分析算法的局限性,我们提出了一些新的HRD诊断观点。我们希望这篇综述将有助于加速分子肿瘤学这一重要领域的新诊断方法的发展。
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引用次数: 0
Influence of antibody-drug conjugate cleavability, drug-to-antibody ratio, and free payload concentration on systemic toxicities: A systematic review and meta-analysis. 抗体-药物共轭物的可裂解性、药物-抗体比率和游离有效载荷浓度对全身毒性的影响:系统回顾与荟萃分析。
IF 7.7 2区 医学 Q1 ONCOLOGY Pub Date : 2024-12-20 DOI: 10.1007/s10555-024-10231-5
Shou-Ching Tang, Carrie Wynn, Tran Le, Martin McCandless, Yunxi Zhang, Ritesh Patel, Nita Maihle, William Hillegass

While in theory antibody drug conjugates (ADCs) deliver high-dose chemotherapy directly to target cells, numerous side effects are observed in clinical practice. We sought to determine the effect of linker design (cleavable versus non-cleavable), drug-to-antibody ratio (DAR), and free payload concentration on systemic toxicity. Two systematic reviews were performed via PubMed search of clinical trials published between January 1998-July 2022. Eligible studies: (1) clinical trial for cancer therapy in adults, (2) ≥ 1 study arm included a single-agent ADC, (3) ADC used was commercially available/FDA-approved. Data was extracted and pooled using generalized linear mixed effects logistic models. 40 clinical trials involving 7,879 patients from 11 ADCs, including 9 ADCs with cleavable linkers (N = 2,985) and 2 with non-cleavable linkers (N = 4,894), were included. Significantly more composite adverse events (AEs) ≥ grade 3 occurred in patients in the cleavable linkers arm (47%) compared with the non-cleavable arm (34%). When adjusted for DAR, for grade ≥ 3 toxicities, non-cleavable linkers remained independently associated with lower toxicity for any AE (p = 0.002). Higher DAR was significantly associated with higher probability of grade ≥ 3 toxicity for any AE. There was also a significant interaction between cleavability status and DAR for any AE (p = 0.002). Finally, higher measured systemic free payload concentrations were significantly associated with higher DARs (p = 0.043). Our results support the hypothesis that ADCs with cleavable linkers result in premature payload release, leading to increased systemic free payload concentrations and associated toxicities. This may help to inform future ADC design and rational clinical application.

虽然理论上抗体药物偶联物(adc)可将大剂量化疗直接传递到靶细胞,但在临床实践中观察到许多副作用。我们试图确定连接体设计(可切割与不可切割)、药物-抗体比(DAR)和游离有效载荷浓度对全身毒性的影响。通过PubMed检索1998年1月至2022年7月间发表的临床试验进行了两项系统评价。符合条件的研究:(1)成人癌症治疗的临床试验,(2)≥1个研究组包括单药ADC,(3)使用的ADC是市售/ fda批准的。数据提取和合并使用广义线性混合效应逻辑模型。纳入了来自11个adc的40项临床试验,涉及7879例患者,其中9例adc具有可切割连接体(N = 2985), 2例adc具有不可切割连接体(N = 4894)。与不可切割连接体组(34%)相比,可切割连接体组(47%)的患者发生≥3级的复合不良事件(ae)明显更多。当根据DAR进行调整时,对于≥3级毒性,不可切割连接子仍然与任何AE的较低毒性独立相关(p = 0.002)。较高的DAR与任何AE≥3级毒性的可能性显著相关。对于任何AE,可切割性状态与DAR之间也存在显著的相互作用(p = 0.002)。最后,较高的测量系统游离有效载荷浓度与较高的dar显著相关(p = 0.043)。我们的研究结果支持这样的假设,即具有可切割连接体的adc会导致有效载荷过早释放,从而导致系统游离有效载荷浓度增加和相关毒性。这可能有助于未来ADC的设计和合理的临床应用。
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引用次数: 0
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