Biomarker Research最新文献

{"title":"Single cell analysis identified IFN signaling activation contributes to the pathogenesis of pediatric steroid-sensitive nephrotic syndrome.","authors":"Qiu-Yu Li, Fei Liu, Xiaoyi Li, Minchao Kang, Linnan Bai, Tong Tong, Chen Zheng, Yanyan Jin, Xiaojing Zhang, Yi Xie, Dandan Tian, Yuanqing Pan, Jingjing Wang, Haidong Fu, Na Jiao, Junnan Wu, JianHua Mao","doi":"10.1186/s40364-025-00790-2","DOIUrl":"10.1186/s40364-025-00790-2","url":null,"abstract":"<p><strong>Background: </strong>Idiopathic nephrotic syndrome (INS) is a prevalent condition whose recurrence leads to multiple adverse effects. Previous studies on INS pathogenesis primarily focused on immune dysregulation, particularly T-cell changes and their correlation with cytokine shifts. Accumulating evidence suggests that B-cell dysfunction also plays a role. Nevertheless, a comprehensive understanding of the mechanisms and effective treatment strategies remains incomplete.</p><p><strong>Methods: </strong>This study investigates changes in gene expressions and cellular interactions of immune cells at a single-cell level using peripheral blood mononuclear cells (PBMCs). And subsequently validated through quantitative PCR (qPCR), enzyme-linked immunosorbent assay (ELISA), and flow cytometry.</p><p><strong>Results: </strong>We identified seven main clusters using unsupervised clustering of 103,213 high-quality single cells. Through unsupervised clustering, patient-specific T cells (IFI44L + CD4 + T cells) that exhibited a pronounced elevation of interferon-stimulated genes (ISGs) is identified. Activation of ISGs and interferon (IFN)-related pathways are also observed in other clusters. Specifically, this study demonstrates that interferon-γ (IFN-γ) plays a crucial role by promoting the interaction between B-cell activating factor (BAFF) and receptors on B cells. This interaction triggers the release of autoantibodies, thereby initiating INS pathogenesis. Furthermore, telitacicept has shown efficacy in treating pediatric patients with frequent relapse NS(FRNS).</p><p><strong>Conclusions: </strong>Overall, our findings underscore the role of interferon and its related pathways in INS pathogenesis, providing novel therapeutic interventions for NS.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"13 1","pages":"77"},"PeriodicalIF":9.5,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144144288","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":"Early kinetics of serum amyloid A predict clinical benefit to first-line chemoimmunotherapy and immunotherapy in advanced non-small cell lung cancer: a retrospective analysis.","authors":"Wei Du, Jianhua Zhan, Kai Wu, Yanming Wang, Li Zhang, Shaodong Hong","doi":"10.1186/s40364-025-00791-1","DOIUrl":"10.1186/s40364-025-00791-1","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) have transformed the treatment landscape for advanced non-small cell lung cancer (NSCLC), yet durable responses remain limited in a subset of patients. Serum amyloid A (SAA), an acute-phase protein linked to systemic inflammation, may reflect dynamic immune responses. This retrospective study analyzed 242 advanced NSCLC patients treated with first-line chemoimmunotherapy or immunotherapy between August 2016 and December 2024. Patients were stratified by early SAA kinetics into flare-responders (initial rise followed by decline), responders (sustained decline), and non-responders. Clinical outcomes, including progression-free survival (PFS) and overall survival (OS), were evaluated using Kaplan-Meier and Cox regression analyses. In the chemoimmunotherapy cohort, SAA flare-responders demonstrated significantly prolonged median PFS (29.8 months, 95% CI: 9.95-49.65; HR: 0.31, 95% CI: 0.15-0.64; p < 0.01) compared to non-responders (7.4 months, 95% CI: 4.67-10.13). Similarly, in the immunotherapy cohort, SAA flare-responders showed superior PFS. (19.9 vs. 2.1 months, HR 0.31, p < 0.01). Multivariate analysis confirmed early SAA kinetics as an independent prognostic factor for both PFS and OS in both treatment groups. Early SAA kinetics serve as a promising non-invasive biomarker for predicting clinical outcomes in advanced NSCLC treated with first-line chemoimmunotherapy or immunotherapy. These findings highlight SAA kinetics as a potential non-invasive biomarker and monitoring SAA dynamics may aid in identifying patients with higher likelihood of clinical benefit; however, prospective studies are required to determine its utility in guiding therapeutic decisions.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"13 1","pages":"76"},"PeriodicalIF":9.5,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12102904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132047","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":"The progress and prospects of targeting the adenosine pathway in cancer immunotherapy.","authors":"Yuying Yang, Lin Zhu, Yantao Xu, Long Liang, Li Liu, Xiang Chen, Hui Li, Hong Liu","doi":"10.1186/s40364-025-00784-0","DOIUrl":"10.1186/s40364-025-00784-0","url":null,"abstract":"<p><p>Despite the notable success of cancer immunotherapy, its effectiveness is often limited in a significant proportion of patients, highlighting the need to explore alternative tumor immune evasion mechanisms. Adenosine, a key metabolite accumulating in hypoxic tumor regions, has emerged as a promising target in oncology. Inhibiting the adenosinergic pathway not only inhibits tumor progression but also holds potential to enhance immunotherapy outcomes. Multiple therapeutic strategies targeting this pathway are being explored, ranging from preclinical studies to clinical trials. This review examines the complex interactions between adenosine, its receptors, and the tumor microenvironment, proposing strategies to target the adenosinergic axis to boost anti-tumor immunity. It also evaluates early clinical data on pharmacological inhibitors of the adenosinergic pathway and discusses future directions for improving clinical responses.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"13 1","pages":"75"},"PeriodicalIF":9.5,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12090549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103166","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":"A plasma 9-microRNA signature for lung cancer early detection: a multicenter analysis.","authors":"Elisa Dama, Tommaso Colangelo, Roberto Cuttano, Rafal Dziadziuszko, Thomas Dandekar, Piotr Widlak, Witold Rzyman, Giulia Veronesi, Fabrizio Bianchi","doi":"10.1186/s40364-025-00787-x","DOIUrl":"10.1186/s40364-025-00787-x","url":null,"abstract":"<p><p>Lung cancer remains the leading cause of cancer-related deaths worldwide. Low-dose computed tomography (LD-CT) screening, combined with effective minimally invasive molecular testing such circulating microRNA, has the potential to reduce the burden of lung cancer. However, their clinical application requires further validation, including studies across diverse patient cohorts from different countries. In this study, we propose a signature of 9 circulating miRNAs derived from a robust multi-platform workflow with a multi-center design, for a total of 276 lung cancer and 451 non-cancer controls, based on the data from two European LD-CT screening cohorts (Poland and Italy). The classification performance of the signature was stable in the two screening cohorts, with AUC=0.78 (SE, 76%; SP, 67%; ACC=70%), and AUC=0.75 (SE, 82%; SP, 68%; ACC=71%) in the Polish and Italian cohorts, respectively. The diagnostic accuracy of the signature was remarkably independent of age, gender, smoking (status and intensity), nodule size, and density. Additionally, the signature demonstrated strong performance in detecting stage I lung cancer, with AUC=0.76 (95%CI: 0.68-0.84), and 0.69 (95%CI: 0.49-0.89) in the Polish and Italian cohorts respectively, with a prediction ability of 63-73%. The signature's ability to discriminate benign nodules was satisfactory, with AUC=0.71 (95%CI: 0.58-0.84). The proposed panel of 9 circulating miRNAs provides a robust and precise diagnostic tool to substantially advance the effectiveness of the LD-CT screening program.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"13 1","pages":"74"},"PeriodicalIF":9.5,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12085043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086934","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":"Insights into KMT2A rearrangements in acute myeloid leukemia: from molecular characteristics to targeted therapies.","authors":"Sara Zehtabcheh, Hamed Soleimani Samarkhazan, Marjan Asadi, Mitra Zabihi, Sahar Parkhideh, Mohammad Hossein Mohammadi","doi":"10.1186/s40364-025-00786-y","DOIUrl":"10.1186/s40364-025-00786-y","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) with KMT2A rearrangements (KMT2A-r) represents a highly aggressive and prognostically unfavorable subtype of leukemia, often resistant to standard treatments and associated with high relapse rates. KMT2A-r, found in 3-10% of adult AML cases, disrupt epigenetic regulation by forming chimeric proteins that activate oncogenic pathways like HOXA and MEIS1. These fusion proteins recruit cofactors such as Menin and DOT1L, driving leukemogenesis through abnormal histone methylation. Diagnosing KMT2A-r AML requires precision, with traditional methods like FISH and RT-PCR being complemented by advanced technologies such as next-generation sequencing (NGS) and machine learning (ML). ML models, leveraging transcriptomic data, can predict KMT2A-r and identify biomarkers like LAMP5 and SKIDA1, improving risk stratification. Therapeutically, there is a shift from chemotherapy to targeted therapies. Menin inhibitors (e.g., Revumenib, Ziftomenib) disrupt the Menin-KMT2A interaction, suppressing HOXA/MEIS1 and promoting differentiation. DOT1L inhibitors (e.g., Pinometostat) show promise in combination therapies, while novel approaches like WDR5 inhibitors and PROTAC-mediated degradation are expanding treatment options. Despite progress, challenges remain, including optimizing minimal residual disease monitoring, overcoming resistance, and validating biomarkers. This review emphasizes the imperative to translate molecular insights into personalized therapeutic regimens, offering renewed hope for patients afflicted by this historically refractory malignancy.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"13 1","pages":"73"},"PeriodicalIF":9.5,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12077025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065092","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":"S100A9 as a potential novel target for experimental autoimmune cystitis and interstitial cystitis/bladder pain syndrome.","authors":"Jiang Zhao, Mi Zhou, Chengfei Yang, Yang-Wuyue Liu, Teng Yang, Bishao Sun, Benyi Li, Ji Zheng, Shuangshuang Dai, Zhenxing Yang, Xiangwei Wang","doi":"10.1186/s40364-025-00763-5","DOIUrl":"https://doi.org/10.1186/s40364-025-00763-5","url":null,"abstract":"<p><strong>Background: </strong>Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic inflammatory disease of the bladder for which no effective therapy is currently available. Understanding the pathogenesis of IC/BPS and identifying effective intervention targets are of great clinical importance for its effective treatment. Our work focuses on elucidating the key targets and underlying mechanisms of IC/BPS.</p><p><strong>Methods: </strong>We established an experimental autoimmune cystitis (EAC) mouse model and generated gene knockout mice to elucidate key mediators triggering chronic inflammatory damage in IC/BPS through using single-cell RNA sequencing, proteomic sequencing, and molecular biology experiments.</p><p><strong>Results: </strong>Our study revealed that the infiltration and activation of macrophages, T cells, and mast cells exacerbated inflammatory bladder damage in both IC/BPS and EAC mice. Notably, cell-cell communication among bladder immune cells was significantly enhanced in EAC mice. Macrophages, as the main cell types altered in EAC mice, received and transmitted the most intensity signalling. Mechanistically, macrophages synthesized and secreted S100A9, which in turn facilitated macrophage polarization and promoted the production of pro-inflammatory cytokines. S100A9 emerged as an important pro-inflammatory and pathogenic molecule in IC/BPS and EAC. Further analysis demonstrated that S100A9 activation enhanced the inflammatory response and exacerbated bladder tissue damage in IC/BPS patients and EAC mice via TLR4/NF-κB and TLR4/p38 signalling pathways. Importantly, inhibition of S100A9 with paquinimod, as well as genetic knockout of S100A9, significantly attenuated the pathological process.</p><p><strong>Conclusions: </strong>S100A9 is an important pro-inflammatory and pathogenic molecule in IC/BPS and EAC. Targeting S100A9-initiated signalling pathways may offer a novel therapeutic strategy for IC/BPS.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"13 1","pages":"72"},"PeriodicalIF":9.5,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12065242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055747","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":"Reliable detection of CNS lymphoma-derived circulating tumor DNA in cerebrospinal fluid using multi-biomarker NGS profiling: insights from a real-world study.","authors":"Veronika Navrkalova, Andrea Mareckova, Samuel Hricko, Viera Hrabcakova, Lenka Radova, Vaclav Kubes, Jakub Porc, Tomas Reigl, Sarka Pospisilova, Jana Kotaskova, Andrea Janikova","doi":"10.1186/s40364-025-00777-z","DOIUrl":"https://doi.org/10.1186/s40364-025-00777-z","url":null,"abstract":"<p><strong>Background: </strong>Diagnosing primary or secondary CNS lymphoma (CNSL) is a clinical challenge due to the limitations of standard biopsy and imaging procedures despite established guidelines. Therefore, accurate biomarkers and analytical methods that are convenient for practical routine use are needed to diagnose and manage these aggressive lymphomas effectively. We evaluated the utility of minimally invasive circulating tumor DNA (ctDNA) detection in a prospective real-world scenario, moving this approach closer to clinical practice.</p><p><strong>Methods: </strong>A total of 164 plasma, cerebrospinal fluid (CSF), and tumor samples from 56 CNSL patients were collected to analyze tumor DNA by the diagnostic next-generation sequencing (NGS) panel LYNX, enabling simultaneous analysis of gene variants, chromosomal aberrations, and antigen receptor rearrangements in targeted regions.</p><p><strong>Results: </strong>The well-known genetic heterogeneity of CNSL was refined with integrative molecular data, showing the most frequent MYD88, PIM1, and KMT2D mutations and a broad spectrum of chromosomal aberrations, reflecting high genomic complexity. The multi-target approach achieved a substantially higher detection rate of CNS infiltration (90%) than tracking a single variant in gene MYD88 (46%). CSF clearly surpasses plasma if applying a routine (non-ultrasensitive) NGS approach and allows for more reliable evidence of CNS involvement than conventional flow cytometry (91% vs. 21%, p < 0.001). Parallel analysis of tumor DNA in both cell-free and cellular DNA from CSF makes the probability of primary or secondary CNS malignancy detection even higher.</p><p><strong>Conclusions: </strong>Our prospective, tissue-agnostic approach highlights the feasibility of ctDNA sequencing by a commonplace and affordable method, offering higher sensitivity to detect CNS infiltration with lymphoma than standard cell-analyzing techniques. We accentuate the benefit of a multi-target NGS approach and adequate CSF sampling to obtain satisfactory diagnostic yield. Less invasive liquid biopsy testing by comprehensive NGS complements standard procedures in the diagnostics and management of CNSL patients, especially when encountering limitations.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"13 1","pages":"71"},"PeriodicalIF":9.5,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12065147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144026713","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":"PAQR5 drives the malignant progression and shapes the immunosuppressive microenvironment of hepatocellular carcinoma by activating the NF-κB signaling.","authors":"Ruida Yang, Huanhuan Wang, Cong Wu, Yu Shi, Hanqi Li, Xinyue Bao, Yuqian Yang, Shaoshan Han, Xue Yang, Jie Tao, Hao Sun, Shaobo Wu, Liankang Sun","doi":"10.1186/s40364-025-00785-z","DOIUrl":"https://doi.org/10.1186/s40364-025-00785-z","url":null,"abstract":"<p><strong>Background: </strong>Progesterone and adipose Q receptor 5 (PAQR5), a membrane receptor characterized by seven transmembrane domains, has been indirectly implicated in pro-carcinogenic activities, though its specific role in hepatocellular carcinoma (HCC) remains to be defined.</p><p><strong>Methods: </strong>This study aimed to elucidate the molecular mechanisms by which PAQR5 facilitates HCC progression and contributes to the immunosuppressive microenvironment through an integrative approach combining multi-omics analysis and experimental validation. Utilizing data from bulk, single-cell, and spatial transcriptomics cohorts, this study systematically assessed the expression patterns, immune landscape, and functional characteristics of PAQR5 across different levels of resolution in HCC.</p><p><strong>Results: </strong>PAQR5 expression was significantly upregulated in tumor tissues and correlated with poor clinical outcomes. Enrichment analysis revealed that PAQR5 activated the NF-κB signaling pathway in HCC. Single-cell transcriptomics identified PAQR5 as predominantly localized within malignant cell clusters, with significant association with NF-κB pathway activation. Spatial transcriptomics further corroborated the alignment of PAQR5 expression with tumor cell distribution. In vitro assays showed elevated PAQR5 levels in HCC cell lines, and silencing PAQR5 significantly suppressed cell proliferation, invasion, epithelial-mesenchymal transition (EMT), and prevented the formation of immunosuppressive microenvironment. In vivo studies demonstrated that targeting PAQR5 attenuated tumorigenic potential, disrupted the invasion-metastasis cascade and inhibited the tumor immune escape. Mechanistically, PAQR5 was found to activate NF-κB signaling by inducing ERK phosphorylation, thereby driving proliferation, invasion, EMT, and immune escape in HCC through the pathway.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"13 1","pages":"70"},"PeriodicalIF":9.5,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12060467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144044456","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":"Advances and challenges in CAR-T cell therapy for head and neck squamous cell carcinoma.","authors":"Sahand Saeidpour Masouleh, Kamyar Nasiri, Ava Ostovar Ravari, Mona Saligheh Rad, Kiarash Kiani, Ali Sharifi Sultani, Seyedeh Tabasom Nejati, Mohsen Nabi Afjadi","doi":"10.1186/s40364-025-00783-1","DOIUrl":"https://doi.org/10.1186/s40364-025-00783-1","url":null,"abstract":"<p><p>Head and neck squamous cell carcinoma (HNSCC) remains among the most aggressive malignancies with limited treatment options, especially in recurrent and metastatic cases. Despite advances in surgery, radiotherapy, chemotherapy, and immune checkpoint inhibitors, survival rates remain suboptimal due to tumor heterogeneity, immune evasion, and treatment resistance. In recent years, Chimeric Antigen Receptor (CAR) T-cell therapy has revolutionized hematologic cancer treatment by genetically modifying T cells to target tumor-specific antigens like CD19, CD70, BCMA, EGFR, and HER2, leading to high remission rates. Its success is attributed to precise antigen recognition, sustained immune response, and long-term immunological memory, though challenges like cytokine release syndrome and antigen loss remain. Notably, its translation to solid tumors, including HNSCC, faces significant challenges, such as tumor microenvironment (TME)-induced immunosuppression, antigen heterogeneity, and limited CAR T-cell infiltration. To address these barriers, several tumor-associated antigens (TAAs), including EGFR, HER2 (ErbB2), B7-H3, CD44v6, CD70, CD98, and MUC1, have been identified as potential CAR T-cell targets in HNSCC. Moreover, innovative approaches, such as dual-targeted CAR T-cells, armored CARs, and CRISPR-engineered modifications, aim to enhance efficacy and overcome resistance. Notably, combination therapies integrating CAR T-cells with immune checkpoint inhibitors (e.g., PD-1/CTLA-4 blockade) and TGF-β-resistant CAR T designs are being explored to improve therapeutic outcomes. This review aimed to elucidate the current landscape of CAR T-cell therapy in HNSCC, by exploring its mechanisms, targeted antigens, challenges, emerging strategies, and future therapeutic potential.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"13 1","pages":"69"},"PeriodicalIF":9.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12044960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144041138","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":"Targeting the chemokine receptor CXCR4 for cancer therapies.","authors":"Ariana Rueda, Naroa Serna, Ramon Mangues, Antonio Villaverde, Ugutz Unzueta","doi":"10.1186/s40364-025-00778-y","DOIUrl":"https://doi.org/10.1186/s40364-025-00778-y","url":null,"abstract":"<p><p>The C-X-C chemokine receptor type 4 (CXCR4) has emerged as a key molecular biomarker for cancer therapies due to its critical role in tumor progression and metastases by displaying a stem cells phenotype. Its overexpression has been observed in more than 20 types of cancers, including solid tumors and hematological malignancies, and it is often associated with tumor aggressiveness and poor prognosis. Being initially recognized as a co-receptor involved in HIV infection, numerous CXCR4-targeting ligands and antagonists, including small molecules, peptides and biologics have been identified over the past decades. While only few of them have been used in the context of cancer therapies, recent biotechnological advancements using CXCR4 as a molecular target are showing significant potential to revolutionize future cancer therapies. Therefore, this review highlights the biotechnological innovations developed for cancer therapy and diagnosis by targeting the chemokine receptor CXCR4. It also discusses future perspectives on emerging therapeutic strategies, ranging from the use of small molecule inhibitors that block receptor signaling to cutting-edge nanocarriers designed for the targeted delivery of innovative drugs and proteins into cancer stem cells, aiming at cell-selective precision nanomedicines.</p>","PeriodicalId":54225,"journal":{"name":"Biomarker Research","volume":"13 1","pages":"68"},"PeriodicalIF":9.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12044942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144026114","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}