Clinical and Experimental Medicine最新文献

{"title":"Correction: Clonal Metamorphosis: Deconstructing MPN Evolution with Single-Cell and Spatial Multi-Omics.","authors":"Muhammad Shahid Iqbal, Abdullah K Alahmari, Mohd Faiyaz Khan, Sadaf Farooqui, Muhammad Zahid Iqbal, Salah-Ud-Din Khan, Nazia Khan, Vidya Devanathadesikan Seshadri, Amr Ali Mohamed Abdelgawwad El-Sehrawy","doi":"10.1007/s10238-026-02261-w","DOIUrl":"10.1007/s10238-026-02261-w","url":null,"abstract":"","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13407714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extranodal involvement defines distinct immune-molecular phenotypes and clinical outcomes in diffuse large b-cell lymphoma.","authors":"Yiliya Ahongjiang, Lihua Qiu, Min Li, Biwen Sun, Huilai Zhang, Chen Tian","doi":"10.1007/s10238-026-02268-3","DOIUrl":"10.1007/s10238-026-02268-3","url":null,"abstract":"<p><p>Extranodal involvement (ENI) is incorporated into routine risk assessment for diffuse large B-cell lymphoma (DLBCL), but treating ENI as a single binary adverse feature may conceal clinically relevant heterogeneity in extranodal burden, anatomical distribution, treatment feasibility, and immune-molecular context. We evaluated ENI as a burden- and site-aware phenotype rather than as a uniform descriptor. We retrospectively studied 710 adults with newly diagnosed DLBCL treated with first-line immunochemotherapy between June 2011 and December 2024. Outcomes were analyzed according to ENI status, number of extranodal sites, and involved organs. Targeted sequencing was available in 176 tumors, and RNA sequencing was performed in 107 quality-controlled tumor samples. Clinical models were interpreted as adjustment models because ENI burden overlaps with established risk factors; site-specific and molecular analyses were prespecified as exploratory and were interpreted with attention to available-case denominators, treatment heterogeneity, sparse subgroups, and multiplicity. ENI was associated with inferior overall survival (OS) and progression-free survival (PFS) in unadjusted analyses. Multisite ENI was enriched for adverse baseline features, including advanced Ann Arbor stage, elevated lactate dehydrogenase (LDH), higher International Prognostic Index (IPI), and impaired performance status. After multivariable adjustment, the independent prognostic contribution of ENI burden was attenuated, indicating substantial clinical overlap with systemic disease burden and host fitness. Several anatomical sites showed candidate adverse signals, but rare-site estimates were limited by small subgroup sizes, wide confidence intervals, and multiple testing. Targeted sequencing and RNA-seq suggested heterogeneous genomic and immune-transcriptional patterns across ENI categories; these results should be regarded as hypothesis-generating because of tissue availability, tumor-only sequencing in many cases, modest molecular sample sizes, and lack of orthogonal immune validation. ENI in DLBCL is best interpreted as a clinically heterogeneous disease descriptor rather than a single uniform prognostic category. ENI burden and anatomical distribution provide useful descriptive and prognostic context, but they should be interpreted alongside established clinical risk, treatment intensity, censoring patterns, tissue-sampling constraints, and molecular ascertainment limitations. Exploratory genomic and immune-transcriptional correlates identified in this study require prospective multicenter validation with harmonized staging, treatment-intensity annotation, matched-normal sequencing, and spatial or cellular immune profiling before ENI-informed biological or therapeutic stratification can be applied clinically.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13451387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of IFIT1 and IFIT3 in systemic lupus erythematosus: modeling a diagnosis and exploring immune regulation.","authors":"Luofei Huang, Jian Shi","doi":"10.1007/s10238-026-02265-6","DOIUrl":"10.1007/s10238-026-02265-6","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by multi-organ involvement and a protracted clinical course. Current diagnostic strategies, which rely heavily on clinical symptoms and serology, are often insufficient for early detection. Therefore, highly accurate diagnostic biomarkers are urgently needed to facilitate early intervention and optimize personalized treatment strategies. D atasets GSE61635 and GSE135779 were integrated to identify differentially expressed genes. Weighted gene co-expression network analysis (WGCNA) was performed to isolate the module with the strongest clinical relevance. Mendelian randomization and single‑cell RNA‑seq were used to identify key disease‑relevant genes. A diagnostic model was then constructed, and gene set variation analysis (GSVA), along with gene set enrichment analysis (GSEA), was conducted to elucidate the underlying molecular pathways. IFIT1 and IFIT3 were identified as 2 core genes highly expressed in monocytes and T cells of SLE patients. Functional enrichment analysis revealed that these genes were enriched in immune-related pathways, metabolic pathways related to inflammation and genomic stability. The diagnostic model showed good accuracy, with an area under the curve (AUC) of 0.974 on the training set and 0.912 on the validation set. IFIT1 and IFIT3 represent promising biomarkers for diagnosing SLE and appear to mediate key immune and metabolic disturbances. Furthermore, the developed model serves as an accurate and reliable instrument for early diagnosis and personalized therapy. Large-scale clinical studies are warranted to further validate these findings and evaluate their clinical application.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated bioinformatic evaluation unveils a cellular senescence gene signature as a poor prognostic factor in hepatocellular carcinoma.","authors":"Shaoyang Lu, Junjie Ma, Xiaodan Wang, Lei Zhang, Jin Lu, Junjie Hu","doi":"10.1007/s10238-026-02258-5","DOIUrl":"10.1007/s10238-026-02258-5","url":null,"abstract":"<p><p>Cellular senescence (CS) plays a crucial role in various diseases, but its role in hepatocellular carcinoma (HCC) remains unclear. CS-related genes were clustered to identify subtypes. A risk score was constructed and validated in three independent cohorts. Associations with clinical characteristics, tumor immune microenvironment, mutation status, heterogeneity, and treatment efficacy were analyzed. Single-cell analysis was used to examine risk score distribution, and machine learning algorithms along with a nomogram were applied to assess prognostic value. Three CS subtypes were identified, with subtype 1 showing the worst prognosis. High risk score was associated with advanced clinical stage and grade, poor prognosis, and an immunosuppressive microenvironment driven by regulatory T cells. It also correlated with higher tumor mutations (notably TP53) and increased heterogeneity. High-risk patients showed poor response to sorafenib and transcatheter arterial chemoembolization (TACE) and may benefit less from immunotherapy. At single-cell level, the risk score was predominantly expressed in malignant hepatocytes and linked to cell stemness. The CS-related risk score is a potential prognostic indicator for poor outcomes in HCC, playing a significant role in tumor progression and offering potential value for clinical diagnosis and prediction of treatment response.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"26 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13522098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of VISTA on peripheral blood mononuclear cells in Systemic lupus erythematosus: association with disease activity and treatment status.","authors":"Afsaneh Enteshari-Moghaddam, Rozita Abolhasan, Meysam Motevasseli, Nasrin Fouladi, Majid Eterafi, Sahar Samemaleki, Hamed Kyanfar, Elham Safarzadeh","doi":"10.1007/s10238-026-02254-9","DOIUrl":"https://doi.org/10.1007/s10238-026-02254-9","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease characterized by autoantibody production and multi-organ involvement due to dysregulated immune responses. Ongoing research aims to understand the underlying mechanisms of this immune dysregulation, with particular interest in immune checkpoint molecules such as VISTA (encoded by the VSIR gene), which exerts context-dependent immunomodulatory effects. We analyzed a large-scale single-cell RNA-seq (scRNA-seq) dataset (GSE174188) comprising 261 samples (162 SLE cases, 99 controls) to investigate VSIR expression patterns across peripheral blood mononuclear cell (PBMC) subsets in SLE versus controls, using bioinformatics tools. Additionally, fresh PBMCs were isolated from SLE patients and healthy controls, and VSIR mRNA levels were quantified by RT-qPCR in treatment-naïve cases and those receiving Prednisolone, Hydroxychloroquine, or supplementary medications. Associations between VSIR expression and clinical/demographic parameters, including disease activity index, were also evaluated. scRNA-seq analysis revealed significantly upregulated VSIR expression in monocytes from SLE patients compared to healthy controls. In contrast, pseudobulk differential expression analysis of the entire PBMC population, corroborated by RT-qPCR on fresh samples, demonstrated downregulation of VSIR in SLE cases overall (log₂ fold change = -1.23). Notably, VSIR expression differed across treatment groups, with the lowest levels observed in treatment-naïve patients and higher levels in those receiving first-line therapies (prednisolone and hydroxychloroquine). Furthermore, VSIR expression exhibited a significant negative correlation with SLE disease activity index. This study demonstrates decreased VSIR expression in the whole PBMC population in SLE patients, suggesting a potential role in disease pathogenesis processes possibly through altered immune checkpoint regulation. Moreover, VSIR expression was associated with treatment status, with higher expression observed in patients receiving standard first-line therapies.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning-based identification of lactate metabolism-associated biomarkers in non-alcoholic fatty liver disease.","authors":"Xiaocui Wang, Xinhan Wang, Liang Zhao, Li Song","doi":"10.1007/s10238-026-02250-z","DOIUrl":"https://doi.org/10.1007/s10238-026-02250-z","url":null,"abstract":"<p><p>To determine lactate metabolism-associated biomarkers for non-alcoholic fatty liver disease (NAFLD). Based on NAFLD datasets from the gene expression omnibus database and lactate metabolism-related genes from GeneCards database, NAFLD-lactate metabolism hub genes (NAFLD-LM HGs) were screened via differential analysis, weighted gene co-expression network analysis and four machine learning algorithms. Their diagnostic efficacy was evaluated; molecular subtyping was performed; single-cell RNA sequencing (scRNA-seq) was subsequently conducted; and validation was finally conducted in NAFLD mouse models. We finally screened out eight NAFLD-LM HGs, namely CCAAT/enhancer-binding protein alpha (CEBPA), flavin containing dimethylaniline monooxygenase 1 (FMO1), insulin-like growth factor-binding protein 1 (IGFBP1), krüppel-like factor 4 (KLF4), low-density lipoprotein receptor (LDLR), myelocytomatosis oncogene (MYC), nuclear receptor subfamily 4 group A member 2 (NR4A2), and thymidylate synthase (TYMS), with a diagnostic rate of 0.798 and an area under the curve of 0.948. These genes drove the molecular heterogeneity in NAFLD patients by modulating of metabolism and immune microenvironment. The results of scRNA-seq clarified that Th17 cells were identified as the most abundant annotated cell subset. Through animal experiments, five genes (LDLR, MYC, IGFBP1, NR4A2, and KLF4) were established to have potential protective effects against NAFLD. Five genes (LDLR, MYC, IGFBP1, NR4A2, KLF4) are identified as \"protective factors\", and their downregulation is associated with NAFLD progression. The remaining three genes (CEBPA, FMO1, TYMS) exhibit inconsistent expression patterns, suggesting bidirectional regulation.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CK2 in triple-negative breast cancer: oncogenic signaling networks and emerging CK2 inhibitor-based combination therapies.","authors":"Navas Shereef Ellyan, Angel Treasa Alex, Usha Yogendra Nayak, Alan Raj, Rahul K","doi":"10.1007/s10238-026-02256-7","DOIUrl":"https://doi.org/10.1007/s10238-026-02256-7","url":null,"abstract":"<p><p>The aggressive and highly heterogeneous subtype of breast cancer, triple-negative breast cancer (TNBC), has a poor response to conventional treatments and a high propensity for metastasis, causing unfavorable clinical outcomes. In TNBC, casein kinase 2 (CK2), a constitutively active serine/threonine kinase, plays a key role in controlling several oncogenic signaling pathways. Aberrant CK2 signaling promotes increased transcription of oncogenes, proliferative signaling, DNA repair, epigenetic regulation, epithelial-to-mesenchymal transition (EMT), and cancer stem cell maintenance. Additionally, CK2 helps maintain tumor redox homeostasis by regulating the balance of zinc and copper and by stabilizing immunological checkpoint proteins such as PD-L1. Due to its pleiotropic effects, CK2 overactivation promotes treatment resistance across TNBC subtypes and accelerates tumor growth. Pharmacological inhibition of CK2 can disrupt these communication networks, making TNBC cells more susceptible to both traditional and targeted treatments. By concurrently suppressing compensatory survival mechanisms, CK2 inhibitors have demonstrated synergistic anticancer benefits when used with chemotherapy, PI3K/AKT/mTOR inhibitors, PARP inhibitors, and immunotherapies. This study highlights the complex role of aberrant CK2 signaling in TNBC progression and examines the therapeutic promise of CK2 inhibitor-based combination therapies to overcome resistance and improve treatment efficacy. Current preclinical and clinical research on next-generation CK2 inhibitors highlights their potential as a novel therapeutic approach for TNBC.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Von Willebrand, factor VIII, and D-dimer levels as predictors of risk and clinical outcomes in acute myeloid leukemia.","authors":"Hanaa Ali El-Sayed, Doaa H Sakr, Mohamed Awad Ebrahim, Reham Alghandour, Eman Eid, May Denewer, Balvinder Saarsalu, Maha Othman, Hanan Azzam","doi":"10.1007/s10238-026-02198-0","DOIUrl":"10.1007/s10238-026-02198-0","url":null,"abstract":"<p><p>Coagulopathies, infection, and CNS infiltration are common complications during induction therapy of acute myeloid leukemia (AML). Early identification of adverse-risk patients may improve outcomes. This study evaluated the predictive value of coagulation markers, von Willebrand Factor antigen (vWF-ag), von Willebrand Factor-ristocetin cofactor (vWF-RCof), antihemophilic factor (FVIII), and D-dimer on risk stratification, severity and outcomes of AML patients. Fifty AML patients treated at Oncology Center Mansoura University hospital, from February 2023 to February 2024 were recruited and stratified into three risk groups favourable, intermediate, and adverse risk groups respectively according to the 2022 European leukemianet (ELN) risk stratification for AML. vWF-ag, vWF: RCof, FVIII, and D-dimer were measured at diagnosis and at remission. Adverse-risk group had the highest median levels of vWF-ag, vWF-RCof, FVIII and D-dimer at, both diagnosis and remission (p < 0.05). All markers significantly declined after remission (p < 0.05). vWF-ag, vWF-RCof, and D-dimer differed significantly among risk groups at both diagnosis and remission. ROC analysis showed that in the adverse-risk group, D-dimer had an AUC of 0.813 (cutoff > 1.6), vWF: Ag 0.780 (> 295), and vWF: RCo 0.761 (> 223). FVIII showed lower predictive value (AUC 0.625). Infection was the most frequent complication, followed by bleeding and thrombosis. Infection correlated with higher vWF: Ag after remission; thrombosis correlated with elevated vWF: Ag at diagnosis and remission and bleeding with lower vWF-ag. CNS infiltration showed no association. vWF-ag, vWF-RCof, and D-dimers may be associated with risk and complications in AML, but these findings require external validation in larger cohorts.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13385243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropeptide Y promotes myocardial fibrosis post myocardial infarction reperfusion through Neuropeptide Y receptor type 1.","authors":"Dinghui Wang, Bo Wei, Chunfeng Cao, Yali Xu, Wen Gou","doi":"10.1007/s10238-026-02253-w","DOIUrl":"https://doi.org/10.1007/s10238-026-02253-w","url":null,"abstract":"<p><p>Although the treatment of ischemic heart disease is becoming increasingly mature, the role of neuropeptide Y (NPY) in the pathophysiology after reperfusion still remains remains unanswered. In our study, we used a mouse model of myocardial ischemia/reperfusion (I/R) injury and demonstrated significant upregulation of NPY and its receptor NPYR1 after reperfusion. Over-expression of NPYR1exacerbates cardiac remodeling, manifested as worsening myocardial fibrosis (p < 0.01) and impaired left ventricular ejection fraction. On the contrary, NPYR1 knockdown weakened fibrosis response and improved cardiac function recovery. These findings were confirmed in HL-1 cell line subjected to hypoxia/reoxygenation model, where fibrotic markers of cardiomyocyte were similarly influenced by NPYR1 modulation. Our research findings indicate that NPY/NPYR1 signaling plays a pivotal role in maladaptive cardiac remodeling post I/R injury and is a promising therapeutic target for alleviating excessive fibrosis.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ncRNA-driven regulation of PD-L1 in breast cancer: mechanisms of immune escape and therapeutic opportunities.","authors":"Amirhossein Mardi, Sajjad Rajabi Moghaddam, Ali Roohi Motlagh, Amirreza Mehmandar-Oskuie","doi":"10.1007/s10238-026-02252-x","DOIUrl":"https://doi.org/10.1007/s10238-026-02252-x","url":null,"abstract":"<p><p>Programmed death-ligand 1 (PD-L1) is an immune checkpoint molecule important in tumor immune evasion acting primarily by inhibiting T cell activation. In breast cancer, PD-L1 is frequently abnormally expressed and associated with tumor progression, metastasis, and poor prognosis. Recent studies have revealed that non-coding RNAs (ncRNAs) including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) are important post-transcriptional regulators of PD-L1. ncRNAs regulate PD-L1 expression through multiple mechanisms, including direct binding to PD-L1 mRNA 3' UTR, acting as competing endogenous RNAs (ceRNAs), altering transcription factor activity, and altering epigenetic modifications. Dysregulation of ncRNAs not only impact PD-L1-mediated immune escape (i.e., cancer immune evasion), but can also remodel the tumor microenvironment (TME) through impact on immune cell infiltration and activity, and alterations to cytokine production. This review provides an overview of current understanding of ncRNAs regulating PD-L1 in breast cancer, specifically their molecular mechanisms, therapeutic potential, and clinical relevance as biomarkers and/or therapeutic targets. The broad ncRNA-PD-L1 regulatory network is complex, and discoveries in this field may create novel avenues for precision immunotherapy and combination strategies in treating breast cancer.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}