Biomarker Research最新文献

{"title":"Neural-tumor interactions: bidirectional regulatory mechanisms and nervous system-targeted tumor therapeutic strategies.","authors":"Yuzhe Huang, Tong Tong, Zhaoyang Zeng, Ming Tan, Hongke Qu, Wei Xiong","doi":"10.1186/s40364-026-00998-w","DOIUrl":"10.1186/s40364-026-00998-w","url":null,"abstract":"<p><p>Neural-tumor crosstalk has emerged as a critical frontier in tumor microenvironment research. Central to this field is the dynamic, bidirectional regulatory network between the nervous system and tumor cells that orchestrates malignant progression. This review focuses on tumors arising outside the central nervous system and their bidirectional interactions with peripheral nerves, summarizing the current evidence on the molecular mechanisms underlying these reciprocal interactions. We first examine how neural components modulate tumorigenesis through the release of neuroactive molecules and proteins that activate oncogenic signaling pathways. In particular, neurons and Schwann cells can transmit protumorigenic signals via paracrine signaling, exosome-mediated communication, and the formation of functional neuroneoplastic synapses. Conversely, tumors can actively \"hijack\" and remodel their neural architecture to promote axonogenesis and neural infiltration while contributing to complications such as cancer pain and paraneoplastic neurological syndromes. We further highlight the pivotal role of neural signaling in reshaping the tumor microenvironment across three interconnected dimensions: the spatial dimension (neural niches), the signaling dimension (bidirectional communication mediated by neuroactive molecules), and the functional dimension (immunometabolic reprogramming). Together, these processes contribute to tumor progression and immune evasion. Building on these insights, therapeutic strategies targeting the neural-tumor interface have shown promising clinical potential. Further characterization of these regulatory networks may identify context-specific drivers of tumorigenesis and progression and inform the development of novel therapeutics targeting neural pathways.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"14 1","pages":""},"PeriodicalIF":14.6,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149031524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular crosstalk of fibroblast-myofibroblast transition in intestinal homeostasis and disease.","authors":"Haodong Yuan, Lin Zhao, Peiqi Xu, Yu Sun, Kai Yin, Shengjun Wang","doi":"10.1186/s40364-026-00997-x","DOIUrl":"10.1186/s40364-026-00997-x","url":null,"abstract":"<p><p>Fibroblasts are central components of the intestinal microenvironment and can acquire a myofibroblast phenotype through fibroblast-to-myofibroblast transition (FMT), a process linked to increased tissue mechanosensitivity and active extracellular matrix (ECM) remodeling. In this way, FMT participates in normal intestinal homeostasis and repair, but it can also contribute to fibrosis and tumor-associated stromal remodeling when sustained. More importantly, FMT is not a passive process but an active reprogramming event in response to physiological demands or pathological conditions. Its regulation is highly complicated by the temporal and spatial coordination of various intestinal cell types, ultimately determining disease onset and progression. In this context, targeting cellular interaction networks and remodeling the pathological microenvironment may provide opportunities to limit or redirect disease-associated stromal remodeling. In this review, we summarize the key intercellular dialogs that regulate FMT during the onset and progression of intestinal disorders and further analyze their regulatory mechanisms. Moreover, we discuss emerging therapies targeting cellular interaction networks to provide a new framework and research focus for treating inflammatory bowel disease (IBD), intestinal fibrosis, and related tumors.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"14 1","pages":""},"PeriodicalIF":14.6,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13579752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic-inflammatory index CTI identifies high-risk early-stage natural killer/T-cell lymphoma and informs a novel prognostic model.","authors":"Qiuhui Jiang, Peng Xu, Huijuan Zhong, Shuhui Fu, Liangjie Wang, Weili Zhao, Shu Cheng, Jie Zha, Bing Xu","doi":"10.1186/s40364-026-00996-y","DOIUrl":"10.1186/s40364-026-00996-y","url":null,"abstract":"<p><strong>Background: </strong>The prognostic heterogeneity of early-stage natural killer/T-cell lymphoma (NKTCL) remains inadequately defined. This study aimed to investigate the prognostic value and potential biological relevance of the metabolic-inflammatory biomarkers in early-stage NKTCL.</p><p><strong>Methods: </strong>We conducted a secondary analysis on 166 patients with early-stage NKTCL from a multicenter clinical trial (NCT02631239). C-reactive protein-triglyceride-glucose Index (CTI) was calculated as: 0.412* Ln (CRP [mg/L]) + Ln (TG [mg/dL] × FPG [mg/dL])/2. Cox proportional hazards models and restricted cubic spline analyses were applied to assess the association and dose-response relationship between CTI and overall survival (OS). Mechanistic insights were explored through animal experiments and clinical lymphocyte-subset analyses. Independent prognostic factors were identified using multivariable Cox regression, and a composite prognostic model incorporating CTI, body mass index (BMI), and albumin (ALB) was subsequently developed and internally evaluated.</p><p><strong>Results: </strong>High CTI was independently associated with inferior OS in patients with early-stage NKTCL, with a significant linear dose-response relationship. Patients with high CTI had a higher incidence of B symptoms and elevated lactate dehydrogenase and β2-microglobulin levels. A simplified CTI-BMI-ALB prognostic model demonstrated moderate predictive performance for 1-, 3-, and 5-year OS, with AUCs of 0.71, 0.71, and 0.69, respectively, and an overall C-index of 0.69 (95% CI: 0.59-0.79). In the present cohort, the CTI-BMI-ALB model showed improved discriminative performance compared with conventional prognostic indices and provided additional survival stratification among patients classified as low-risk or favorable-risk by these indices within this cohort. In vivo experiments showed that the Gubra-Amylin NASH diet-induced metabolic-inflammatory state with elevated CTI levels was associated with accelerated lymphoma progression, reduced intratumoral CD8⁺ T-cell infiltration, and increased proportions of Tregs and M2 macrophages. Consistently, clinical lymphocyte-subset analysis confirmed Treg enrichment in patients with high CTI and a positive association between CTI and the proportion of Tregs.</p><p><strong>Conclusion: </strong>CTI is an independent prognostic biomarker in early-stage NKTCL, reflecting systemic metabolic-inflammatory and immune dysregulation. The CTI-BMI-ALB model, which integrates inflammatory, nutritional, and metabolic dimensions, showed potential for complementary risk stratification beyond conventional prognostic indices and warrants further validation before broader clinical application.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"14 1","pages":""},"PeriodicalIF":14.6,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13579890/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biohybrid M13 phage backpacks for active blood-brain barrier traversal and precision central nervous system leukemia treatment.","authors":"Wei Wu, Cheng-Ling Zhang, Yu-Ling Yang, Xiaoyuan Chen, Xi Zhang, Xue Dong","doi":"10.1186/s40364-026-01000-3","DOIUrl":"10.1186/s40364-026-01000-3","url":null,"abstract":"<p><p>Central nervous system (CNS) leukemia remains a major clinical challenge in acute lymphoblastic leukemia, largely due to the restrictive nature of the blood-brain barrier (BBB), which severely limits therapeutic delivery and contributes to high relapse rates and poor prognosis. Here, we report ALB-phage, a bioengineered anti-leukemia backpack-phage system designed for active BBB navigation and intracranial drug delivery. M13 bacteriophages were genetically engineered to display BBB-homing ligands, forming a high-aspect-ratio biological transport platform (BTP). A leukemia-targeting therapeutic backpack (L-Pak) was constructed by encapsulating methotrexate within lipid nanoparticles fused with leukemia cell membranes, enabling homotypic targeting. The L-Pak was conjugated to the BTP via a matrix metalloproteinase-responsive PLGVR linker, allowing selective cleavage within the cerebrospinal fluid. Owing to its filamentous morphology, ALB-phage achieved efficient BBB translocation predominantly through energy-dependent macropinocytosis with an additional contribution from clathrin-mediated endocytosis. Both in vitro and in vivo studies demonstrate that ALB-phage effectively penetrates the BBB and selectively eradicates leukemia blasts, resulting in marked tumor suppression and a significant extension of median survival from 29 to 40 days in cell-line-derived xenograft models. Collectively, this M13 bacteriophage-based all-in-one platform integrates targeted BBB penetration with homology-mediated cytotoxicity, offering a promising strategy for the treatment of CNS leukemia and other central nervous system malignancies.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"14 1","pages":""},"PeriodicalIF":14.6,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13579763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148984363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AI-driven precision immunotherapy: emerging trends from AACR 2026.","authors":"Yani Chen, Ming Chen, Yiqing Xi, Yun Xia, Siyuan Ma, Baoxiang Chen","doi":"10.1186/s40364-026-00995-z","DOIUrl":"10.1186/s40364-026-00995-z","url":null,"abstract":"<p><p>Artificial intelligence (AI) has become a pivotal driver of innovation in cancer immunotherapy through large-scale biological data modeling, multimodal information integration, and advanced machine learning approaches. At the AACR Annual Meeting 2026, AI-based frameworks demonstrated broad applications across the immunotherapy continuum, including response prediction, patient stratification, neoantigen identification, and therapeutic development. An array of studies has transcended conventional single-biomarker paradigms, leveraging multimodal clinical and molecular datasets to construct biologically interpretable representations of tumor-immune ecosystems. Taken together, these advances signal a shift from reductionist biomarker-based prediction toward integrative, data-driven precision immunotherapy, fundamentally reshaping therapeutic stratification and target discovery and establishing artificial intelligence as a central driver of the conceptual and practical transformation of cancer immunotherapy.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"14 1","pages":""},"PeriodicalIF":14.6,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148914316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond hypoxia and ccRCC: the expanding universe of VHL novel targets and next-generation therapeutics.","authors":"Ruiyi Deng, Boyuan Wang, Mingrui Zou, Kaiyuan Mao, Jiaheng Shang, Jianhui Qiu, Jingcheng Zhou, Hua Xu, Xin Ma, Yizhou Wang, Lin Cai, Kan Gong","doi":"10.1186/s40364-026-00986-0","DOIUrl":"10.1186/s40364-026-00986-0","url":null,"abstract":"<p><p>The von Hippel-Lindau (VHL) gene encodes the core substrate-recognition subunit of the Cullin2-RING E3 ubiquitin ligase complex, regulating cellular oxygen sensing and proteostasis. While targeting the canonical VHL-hypoxia-inducible factor (HIF) axis (e.g. belzutifan) has improved advanced clear cell renal cell carcinoma (ccRCC) management, intrinsic non-responsiveness and acquired resistance to HIF-2α inhibitors present major clinical limitations. Expanding beyond the HIF-centric paradigm reveals a broader network of non-canonical VHL targets, offering new opportunities for therapeutic development across ccRCC and pan-cancer contexts. This review provides an evidence-graded synthesis of novel VHL targets spanning epigenetic regulation (e.g. ZHX2, SETDB1, METTL3/METTL14), metabolic reprogramming (e.g. NDRG3, TFAM), extracellular matrix architecture (e.g. fibronectin, COL4A2), and immune modulation (e.g. TBK1). Supporting evidence across these targets ranges from direct biochemical ubiquitination to indirect downstream observations, derived predominantly from preclinical cell-line and xenograft models. Disruption of VHL and these non-HIF networks contributes to oncogenesis across diverse malignancies. Translating these mechanistic insights catalyzes two distinct therapeutic modalities. For VHL-deficient malignancies, selectively intercepting unshielded downstream effectors with small-molecule inhibitors provides rational, vulnerability-targeted salvage strategies. Conversely, in VHL-proficient malignancies, the exceptional chemical tractability of VHL has been repurposed by proteolysis targeting chimeras (PROTACs). VHL-recruiting PROTACs hijack operational ligase machinery to degrade targeted oncogenic drivers, including some previously \"undruggable\" oncogenes. These next-generation degraders offer potential biomarker-driven strategies to overcome current therapeutic bottlenecks in ccRCC and other associated malignancies. However, current evidence derives predominantly from in vitro and animal models. Realizing the clinical potential of VHL-targeted strategies requires addressing key unresolved questions regarding substrate directness, tissue tropism, and resistance trade-offs. Further investigating these core mechanistic and pharmacological bottlenecks will be essential to guide next-generation therapies in VHL-associated malignancies.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"14 1","pages":""},"PeriodicalIF":14.6,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13560369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148921842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory bone marrow microenvironment impairs the therapeutic effect of daratumumab-lenalidomide in multiple myeloma.","authors":"Wenwen Cheng, Silvia Gaggero, Lama Hasan Bou Issa, Aïcha Ouelkdite, Guillaume Escure, Adeline Cozzani, Yanick Njosse Tchantchou, Noémie Carlier, Emilie Wauquier, Gauthier Decool, Rémi Tilmont, Benjamin Podvin, Malo Leprohon, Mojtaba Shekarkar, Léa Fléchon, Angélina Kasprowicz, Sophie Groux-Degroote, Jérôme Moreaux, Bertrand Arnulf, Jill Corre, Céline Villenet, Ludovic Martinet, Xavier Leleu, Martin Figeac, Thierry Facon, Wenfei Jin, Suman Mitra, Salomon Manier","doi":"10.1186/s40364-026-00992-2","DOIUrl":"10.1186/s40364-026-00992-2","url":null,"abstract":"<p><p>Daratumumab-lenalidomide (DR) combination therapy improves multiple myeloma (MM) outcomes, yet some patients respond poorly. We examined 21 DR pre-treatment samples from the IFM2017-03 phase 3 trial using single-cell and bulk multiomics approaches to identify determinants of response. Analysis of the bone marrow environment revealed a coordinated inflammatory state across immune and myeloma cells associated with DR resistance. We identified upregulated NF-κB signaling genes in monocytes of non-responders, alongside increased proinflammatory ISG + T cells and attenuated NK cell CD16 expression, suggesting an impairment of antibody-dependent cellular cytotoxicity essential for daratumumab efficacy. Concurrently, myeloma cells displayed enhanced NF-κB activation, supporting convergent tumor and immune inflammatory programs. We further developed an eight-gene NF-κB-related signature that robustly predicted treatment response in independent bone marrow (n = 28, AUC = 0.81) and peripheral blood (n = 40, AUC = 0.77) samples. Our study underscores an NF-κB-associated inflammatory axis underlying poor DR response and suggests that targeting inflammatory pathways a potential therapeutic avenue warranting further investigation.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"14 1","pages":""},"PeriodicalIF":14.6,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13546506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148898311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating molecular subtypes, genomics and functional dependencies to identify context-specific therapeutic vulnerabilities in small cell lung cancer.","authors":"Ilaria Cassotti, Vito Fiume, Paolo Gandellini, Clelia Tiziana Storlazzi","doi":"10.1186/s40364-026-00991-3","DOIUrl":"10.1186/s40364-026-00991-3","url":null,"abstract":"<p><p>Small cell lung cancer is one of the most aggressive malignancies, characterized by rapid tumor growth, early metastatic spread and extremely poor survival. Although most patients initially respond to platinum-based chemotherapy, relapse is almost inevitable and treatment options at recurrence remain limited. The recent introduction of immune checkpoint inhibitors has provided only modest clinical benefit, largely due to the fact that these tumors are immunologically cold. These limitations highlight the urgent need to better understand the molecular features of small cell lung cancer in order to identify more effective therapeutic strategies. In this review, we summarize current knowledge of the molecular landscape of small cell lung cancer, with particular emphasis on transcriptome-based classifications that have identified four major molecular subtypes defined by distinct transcriptional regulators and gene expression programs. We discuss how these classifications have improved the biological understanding of the disease and stimulated efforts to develop subtype-specific therapeutic strategies. At the same time, we highlight important limitations of this framework, including the remarkable transcriptional plasticity of tumor cells, which allows dynamic transitions between subtypes and may contribute to therapeutic resistance. To address these challenges, we examine additional molecular features that may represent more stable vulnerabilities, including recurrent genomic alterations, such as the widespread loss of tumor suppressor genes or oncogene amplifications through extrachromosomal DNA. We also discuss emerging approaches aimed at identifying novel context-specific cancer dependencies, including genome-scale functional screens in vitro and in vivo and genetic restraint analyses. Finally, we consider the growing potential of liquid biopsy strategies, which exploit the high level of circulating tumor DNA in patients with this disease to detect clinically relevant genomic alterations and monitor tumor evolution. Overall, this review highlights both the opportunities and challenges associated with molecular stratification in small cell lung cancer. The integration of transcriptional classifications with genomic and functional approaches may help identify more robust therapeutic vulnerabilities and guide the development of more effective treatments for this highly aggressive disease.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"14 1","pages":""},"PeriodicalIF":14.6,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13546517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148898336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping brain volume changes in the zQ175DN mouse model of Huntington's disease: a longitudinal MRI study.","authors":"Nicholas Vidas-Guscic, Tamara Vasilkovska, Stefanie Pluym, Joëlle van Rijswijk, Johan Van Audekerke, Haiying Tang, Ignacio Muñoz-Sanjuán, Dorian Pustina, Roger Cachope, Annemie Van der Linden, Daniele Bertoglio, Marleen Verhoye","doi":"10.1186/s40364-026-00971-7","DOIUrl":"10.1186/s40364-026-00971-7","url":null,"abstract":"<p><strong>Background: </strong>Huntington's disease (HD) is a progressive neurodegenerative disease affecting motor and cognitive abilities, as well as exhibiting psychiatric manifestations. Studies in people with HD (PwHD) consistently report atrophy of the caudate and putamen as an early pathological event and is therefore considered an early biomarker. Investigating whether similar phenotypic features are apparent in rodent HD models is important since it could have translational potential in evaluating the efficacy of novel therapeutic strategies.</p><p><strong>Methods: </strong>We used high-resolution anatomical images to longitudinally investigate brain morphology in the zQ175DN heterozygous mouse model (HET) and wildtype littermates (WT) at 3, 6, and 10 months of age (M), which reflect different stages of phenotypic progression. We investigated volumetric alterations using semi-automatic segmentations of HD on relevant regions-of-interest (striatum, cerebellum, corpus callosum, cerebral cortex, ventricles, and total brain volume) and whole brain voxel-wise Tensor Based Morphometry (TBM) analysis.</p><p><strong>Results: </strong>The striatum showed the earliest progressive lower absolute volume in HET mice compared to WT, starting from 3 M, followed by lower absolute volume of cortex and corpus callosum concomitantly at 6 and 10 M. TBM highlighted lower relative local volume in the rostral-medial striatum at all ages, and in cerebral cortex in HET mice at 6 and 10 M. A bigger relative local volume in the cerebellum was observed at all ages in HET mice, and in the globus pallidus, substantia nigra, at 6 and 10 M.</p><p><strong>Conclusions: </strong>Overall, this study revealed key structural abnormalities that resemble the natural history of PwHD. Hence, analysis of brain structure through MRI in the zQ175DN heterozygous mouse model holds potential for testing disease-modifying treatments expected to slow down or prevent structural degeneration.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"14 1","pages":""},"PeriodicalIF":14.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148875636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating global clinical trials and development trends of antibody-drug conjugates.","authors":"Jintao Hu, Cong Lai, Junjie Wang, Zi Yan, Zhihan Yuan, Chunnuan Deng, Wang He, Cheng Liu, Kewei Xu","doi":"10.1186/s40364-026-00994-0","DOIUrl":"10.1186/s40364-026-00994-0","url":null,"abstract":"<p><p>Antibody-drug conjugates (ADCs) represent a breakthrough in tumor-targeted therapy, showing promise in both solid tumors and hematological malignancies. By 1 September 2025, more than 370 ADC candidates had entered clinical development, 17 unique products had received at least one regulatory approval worldwide, and more than 150 candidates had been discontinued. This study analyzes 3,077 ADC trials from Citeline Trialtrove, revealing that most trials are concentrated in the United States and China. At the data cutoff, 35% of trials were ongoing and 12% were classified as terminated in Trialtrove. ADC trials primarily focused on solid tumors, with brentuximab vedotin, disitamab vedotin, and gemtuzumab ozogamicin being the most frequently investigated agents. Early-phase trials predominated, whereas Phase III and IV trials were less frequent. EGFR, BRCA1, and TP53 were frequently recorded across trial-design and outcome-related fields. Future research should focus on advancing later-phase trials, refining safety and efficacy, and exploring new therapeutic targets with continued biomarker integration.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"14 1","pages":""},"PeriodicalIF":14.6,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13523232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148852022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}