Clinical & Translational Oncology最新文献

{"title":"Stereotactic radiosurgery vs. fractionated radiotherapy for large vestibular schwannomas: should FSRT be the preferred treatment?","authors":"Berna Akkus Yildirim, Caglayan Selenge Beduk Esen, Omer Faruk Pekgoz, Bengisu Unver, Tanju Berber, Necla Gurdal, Emre Uysal","doi":"10.1007/s12094-024-03790-0","DOIUrl":"10.1007/s12094-024-03790-0","url":null,"abstract":"<p><strong>Introduction: </strong>To evaluate the effect of fractionation and prognostic factors on local control (LC) in the treatment of vestibular schwannoma (VS).</p><p><strong>Methods: </strong>The medical records of 104 patients with vestibular schwannoma who were treated with stereotactic radiosurgery (SRS) from January 2015 to September 2023 were retrospectively collected. SRS was performed using Cyberknife^® robotic lineer accelerator. The primary endpoint of this study was LC rates. The chi-square test or Fischer's exact test, where appropriate, was used to compare progression rates in patients with small (< 20 cc) and large tumors (≥ 20 cc) which were treated in different fractionation schemes.</p><p><strong>Results: </strong>The median total prescribed dose was 18 Gy (range, 12-30 Gy). With a median 54.8 month follow-up period (range, 3.4-111.9 month), 12 (12%) patients had progressive disease. Regression in tumor size, and stable disease was observed in 49 (47%) and 43 (41%) patients, respectively. The 3-y LC rate was 89% in all cohort and similar between patients who received SRS in 1, 3, and 5 fractions (p = 0.074). LC rates were slightly lower in patients with large tumors than those with small tumors (83% vs 94%, p = 0.200). Patients with large tumors (≥ 20 cc) which was treated with SRS in 1 fraction had a higher rate of progression compared to patients with small tumors (< 20 cc) (100% vs 0%, p = 0.006). But there was no difference between progression rates in large and small tumors, which were treated in 3, and 5 fractions (p = 0.100 and p = 1.000, respectively). No prognostic factors were found to predict tumor progression.</p><p><strong>Conclusion: </strong>Both SRS and fractionated stereotactic radiotherapy (FSRT) provides high LC in patients with VS, however, FSRT may be preferred for large tumors due to higher LC rates compared to single fraction SRS.</p>","PeriodicalId":50685,"journal":{"name":"Clinical & Translational Oncology","volume":" ","pages":"3198-3203"},"PeriodicalIF":2.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Axillary lymph node management strategies in cN + breast cancer patients after neoadjuvant chemotherapy.","authors":"Min Gao, Xiaoxi Chen, Ling Xu","doi":"10.1007/s12094-024-03817-6","DOIUrl":"10.1007/s12094-024-03817-6","url":null,"abstract":"<p><p>With the widespread use of neoadjuvant chemotherapy (NAC), the optimal management strategy for axillary lymph nodes following chemotherapy has become a hot topic of discussion. For patients with clinically positive axillary lymph nodes (cN +) (defined as axillary lymph nodes confirmed positive by pathology before NAC), axillary lymph node dissection (ALND) remains the current standard treatment. However, there is still no consensus on whether sentinel lymph node biopsy (SLNB) and other local axillary treatments following NAC can safely replace ALND to reduce injury and complications. This article provides a narrative review of strategies for managing axillary lymph nodes in this patient population.</p>","PeriodicalId":50685,"journal":{"name":"Clinical & Translational Oncology","volume":" ","pages":"2769-2777"},"PeriodicalIF":2.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142840060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LAG-3 and TIM-3 expression in melanoma and histopathological correlation: a single-center study.","authors":"Mine İlayda Şengör Aygün, Özben Yalçın","doi":"10.1007/s12094-024-03836-3","DOIUrl":"10.1007/s12094-024-03836-3","url":null,"abstract":"<p><strong>Introduction: </strong>Melanomas originate from melanocytes and can be fatal. Surgical excision is primary, but due to potential rapid metastases, additional therapies are crucial. Our study aimed to assess Lymphocyte-activation gene 3 (LAG-3) and T-cell immunoglobulin and mucin domain 3 (TIM-3) expression in melanoma, exploring their relationships with survival and clinicopathological data.</p><p><strong>Methods: </strong>The study included 64 melanoma skin excision samples examined at the Pathology Department of Saglik Bilimleri University Prof. Dr. Cemil Tascioglu City Hospital between 2017-2023. LAG-3 and TIM-3 immunohistochemical studies were conducted by two pathologists to assess their expression rates and intensities. The study investigated correlations between these markers and epidemiological, clinical, and histopathological features of the cases. Statistical analysis was performed using SPSS 27, with significance levels set at p<0.05.</p><p><strong>Results: </strong>There was a significant association between LAG-3 and TIM-3 expressions (p: 0.001). LAG-3 expression correlated significantly with progression free survival (PFS) and overall survival (OS) rates (p: 0.020; p: 0.023). However, TIM-3 expression did not show significant correlations with PFS and OS times (p: 0.726; p: 0.903). Both LAG-3 and TIM-3 expressions were elevated in deceased patients (p: 0.001; p: 0.042). LAG-3 positivity was identified as an independent risk factor for OS, regardless of disease stage (p: 0.008).</p><p><strong>Conclusions: </strong>Research on immune checkpoint inhibitors has intensified in recent years. The expression of LAG-3 and TIM-3 is associated with poor prognosis in melanomas. Combined treatments targeting these markers may be beneficial in the treatment of this disease.</p>","PeriodicalId":50685,"journal":{"name":"Clinical & Translational Oncology","volume":" ","pages":"3084-3099"},"PeriodicalIF":2.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142923654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting breast tumor extracellular matrix and stroma utilizing nanoparticles.","authors":"Faris Anad Muhammad, Farag M A Altalbawy, Viralkumar Mandaliya, Shelesh Krishna Saraswat, M M Rekha, Damanjeet Aulakh, Mamata Chahar, Morug Salih Mahdi, Mohammed Adil Jaber, Merwa Alhadrawi","doi":"10.1007/s12094-024-03793-x","DOIUrl":"10.1007/s12094-024-03793-x","url":null,"abstract":"<p><p>Breast cancer is a complicated malignancy and is known as the most common cancer in women. Considerable experiments have been devoted to explore the basic impacts of the tumor stroma, particularly the extracellular matrix (ECM) and stromal components, on tumor growth and resistance to treatment. ECM is made up of an intricate system of proteins, glycosaminoglycans, and proteoglycans, and maintains structural support and controls key signaling pathways involved in breast tumors. ECM can block different drugs such as chemotherapy and immunotherapy drugs from entering the tumor stroma. Furthermore, the stromal elements, such as cancer-associated fibroblasts (CAFs), immune cells, and blood vessels, have crucial impacts on tumor development and therapeutic resistance. Recently, promising outcomes have been achieved in using nanotechnology for delivering drugs to tumor stroma and crossing ECM in breast malignancies. Nanoparticles have various benefits for targeting the breast tumor stroma, such as improved permeability and retention, extended circulation time, and the ability to actively target the area. This review covers the latest developments in nanoparticle therapies that focus on breast tumor ECM and stroma. We will explore different approaches using nanoparticles to target the delivery of anticancer drugs like chemotherapy, small molecule drugs, various antitumor products, and other specific synthetic therapeutic agents to the breast tumor stroma. Furthermore, we will investigate the utilization of nanoparticles in altering the stromal elements, such as reprogramming CAFs and immune cells, and also remodeling ECM.</p>","PeriodicalId":50685,"journal":{"name":"Clinical & Translational Oncology","volume":" ","pages":"2801-2824"},"PeriodicalIF":2.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142848334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biogenesis and functional implications of extracellular vesicles in cancer metastasis.","authors":"Sneha Sekar, Sandhya Srikanth, Anirban Goutam Mukherjee, Abilash Valsala Gopalakrishnan, Uddesh Ramesh Wanjari, Balachandar Vellingiri, Kaviyarasi Renu, Harishkumar Madhyastha","doi":"10.1007/s12094-024-03815-8","DOIUrl":"10.1007/s12094-024-03815-8","url":null,"abstract":"<p><p>Extracellular vesicles (EVs) play a crucial role in the complex process of cancer metastasis by facilitating cellular communication and influencing the microenvironment to promote the spread and establishment of cancer cells in distant locations. This paper explores the process of EV biogenesis, explaining their various sources that range from endosomal compartments to plasma membrane shedding. It also discusses the complex mechanisms that control the sorting of cargo within EVs, determining their chemical makeup. We investigate the several functions of EVs in promoting the spread of cancer to other parts of the body. These functions include influencing the immune system, creating environments that support the formation of metastases before they occur, and aiding in the transformation of cells from an epithelial to a mesenchymal state. Moreover, we explore the practical consequences of EV cargo, such as nucleic acids, proteins, and lipids, in influencing the spread of cancer cells, from the beginning of invasion to the creation of secondary tumor sites. Examining recent progress in the field of EV-based diagnostics and treatments, we explore the potential of EVs as highly promising biomarkers for predicting the course of cancer and as targets for therapeutic intervention. This review aims to provide a complete understanding of the biology of EVs in the context of cancer metastasis. By unravelling the nuances of EV biology, it seeks to pave the way for new tactics in cancer detection, treatment, and management.</p>","PeriodicalId":50685,"journal":{"name":"Clinical & Translational Oncology","volume":" ","pages":"2913-2935"},"PeriodicalIF":2.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142866153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PMN-MDSCs are responsible for immune suppression in anti-PD-1 treated TAP1 defective melanoma.","authors":"Xiao Zhang, Kaijun Sun, Bingzheng Zhong, Likun Yan, Pengrui Cheng, Qiang Wang","doi":"10.1007/s12094-024-03840-7","DOIUrl":"10.1007/s12094-024-03840-7","url":null,"abstract":"<p><strong>Introduction: </strong>The transporter associated with antigen processing (TAP) is a key component of the classical HLA I antigen presentation pathway. Our previous studies have demonstrated that the downregulation of TAP1 contributes to tumor progression and is associated with an increased presence of myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment. However, it remains unclear whether the elevation of MDSCs leads to immune cell exhaustion in tumors lacking TAP1. In this study, we established mouse models of tumors with TAP1 deficiency, and we employed PMN-MDSC depletion to investigate their impact on the immune microenvironment within the tumors. We found that MDSC depletion significantly altered the immune-suppressive effects of TAP1-deficient tumor when anti-PD-1 treatment was administered. Targeting PMN-MDSC may be a promising therapeutic strategy for the treatment of tumors with TAP1 deficiency during ICB treatment.</p><p><strong>Methods: </strong>Immunohistochemistry (IHC) was conducted to assess TAP1 expression in mouse melanoma tissues. Ly6G, F4/80, and NKp46 markers were detected in B16 parental and TAP1 knockout tissues, respectively. To enhance anti-tumor immunity, hyperthermia-treated B16F10 WT cell suspension was injected prior to tumor cell introduction. Subsequently, we established B16F10 TAP1 knockout and WT melanoma mouse models. Tumors were collected, and the immune microenvironment was monitored accordingly. Anti-Ly6G antibody was administered to deplete polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs). Finally, flow cytometry analysis for immune infiltration, quantitative PCR for cytokine levels, and immunofluorescence assays were performed to analyze the immune response.</p><p><strong>Results: </strong>The level of Ly6G+ cell infiltration was significantly higher in samples exhibiting low TAP1 expression, while no differences were observed in the infiltration of F4/80+ cells or NKp46+ cells. Furthermore, the immune-suppressive effects associated with PMN-MDSCs were reversed following their elimination; this resulted in an increase in CD8+ T cells and a higher ratio of CD8+ T cells to Tregs, while the infiltration of innate immune cells remained unaffected. Functional markers of these immune cells indicated an active anti-tumoral immune response following the removal of PMN-MDSCs. Quantitative PCR analysis indicated elevated levels of TNF-α and IL-6, accompanied by decreased levels of TGF-β in the tumor microenvironment of TAP1.</p><p><strong>Conclusions: </strong>Our data indicate that myeloid-derived suppressor cells (PMN-MDSCs) play an essential role in creating a tumorigenic immune microenvironment in TAP1 knockout tumors. Therefore, targeting PMN-MDSCs may become a promising therapeutic strategy for the treatment of tumors with TAP1 deficiency during ICB treatment.</p>","PeriodicalId":50685,"journal":{"name":"Clinical & Translational Oncology","volume":" ","pages":"3073-3083"},"PeriodicalIF":2.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143015424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemotherapy-associated mutational process signature and genomic alterations associated with outcome in metastatic pancreatic cancer.","authors":"Kaiqiang Wang, Linqiang Zhang, Qingkui Li, Qinghua Wang, Zhijia Jiang, Yaqing Wei, Tonghe Zhang, Zhaoyang Li, Zhan Jiang, Huitang Yang, Yandong Cai, Guoju Fan, Bo Chen, Hongwei Zhang, Yankui Li, Jinjin Sun","doi":"10.1007/s12094-025-03975-1","DOIUrl":"https://doi.org/10.1007/s12094-025-03975-1","url":null,"abstract":"<p><strong>Objective: </strong>Metastatic pancreatic cancer (mPAC) carries a dismal prognosis, and effective prognostic biomarkers are critically needed. This study aims to explore novel molecular prognostic markers for mPAC from the perspective of somatic mutations.</p><p><strong>Methods: </strong>We integrated clinical data and somatic mutation profiles from 820 mPAC patients. Prognosis-associated molecular markers were systematically explored from three perspectives: mutational process signatures, mutation activity-driven molecular subtypes, and genomic variations.</p><p><strong>Results: </strong>The median overall survival was 11.1 months (95% CI: 9.92-12.6). Liver metastasis was the most common site and associated with worse prognosis. Tumor mutational burden (TMB) and fraction genome alteration (FGA) were favorable prognostic biomarkers. Non-negative matrix factorization identified three distinct mutational process signatures (SBS1, SBS11, and SBS29). Notably, the presence of the temozolomide-associated signature (SBS11, characterized by C > T substitutions) was associated with improved survival. Consensus clustering of mutational activity defined seven molecular subtypes, one of which (Cluster 4) demonstrated the most favorable prognosis. Genomic profiling revealed that patients harboring KRAS p.G12V mutations had the poorest survival outcomes and significantly reduced immunogenicity. Furthermore, copy-number deletions in KRAS, AKT2, and MYC were identified as biomarkers of adverse prognosis.</p><p><strong>Conclusions: </strong>By deciphering the somatic mutational landscape of mPAC, this study identified potential molecular biomarkers associated with survival outcomes, providing a scientific foundation for prognostic prediction and informing clinical treatment strategies for mPAC.</p>","PeriodicalId":50685,"journal":{"name":"Clinical & Translational Oncology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144509269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiota interaction with Tregs: a target for colitis.","authors":"Keywan Mortezaee","doi":"10.1007/s12094-025-03974-2","DOIUrl":"https://doi.org/10.1007/s12094-025-03974-2","url":null,"abstract":"<p><p>Gut-resident microbiota associate with host immune system to promote homeostasis, and regulatory T cells (Tregs) are critical in the maintenance of immune balance. Tregs have immunosuppressive activity, and their presence hampers the development of inflammatory diseases. This review aims to unravel microbiome impact on Tregs in bowel inflammation and harnessing such interaction to combat colitis as a separate disease or a consequence of immune checkpoint inhibitor (ICI) therapy of cancer. Short-chain fatty acids (SCFAs) are microbial-derived metabolites associated positively with Treg generation and maintenance and being effective for hampering bowel inflammation. Treg induction shapes gut microbiota profile and support microorganism colonization in their niche and protect the host from inflammation, while suppression of Treg differentiation and activity directs microbiota-induced Th17 expansion and inducing inflammation. Thus, balancing Treg representation with Th17 cells and Treg reprogramming through manipulation of gut microbiota can offer therapy. Microbiota epithelial attachment/detachment and interaction with antigen-presenting cells (APCs) are important for the final fate of T cell signature. Fecal microbial transplantation (FMT) is a strategy for promoting normobiosis and represents a navel approach to targeting colitis. FMT with appropriate microbiota from healthy donors can reinforce microbial diversity, density and persistence to enrich their environment with transforming growth factor (TGF)-β, induce IL-10 producing APCs and reinforce gut barrier, with all these being effective for recovering Tregs, restoring intestinal homeostasis and hampering colitis. ICI therapy of cancer may predispose subjects to colitis due to the impact on microbiome and reducing Treg population. FMT promotes local Treg reorchestration, being advantageous in cancer patients.</p>","PeriodicalId":50685,"journal":{"name":"Clinical & Translational Oncology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144499072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UGT1A6 in pancreatic cancer: a promising prognostic biomarker and therapeutic target.","authors":"Xue-An Lu, Yan-Nan Pan, Chen-Jun Xie, Qing-Wen Wang, Shi-Wei Xu, Qin Wang, Youzhao He, Lei-Sheng Wang, Yong Mao, Hao Hu","doi":"10.1007/s12094-025-03976-0","DOIUrl":"https://doi.org/10.1007/s12094-025-03976-0","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to explore the role of the UDP glucuronosyltransferase 1 family, polypeptide A6 (UGT1A6), in pancreatic cancer, focusing on its expression patterns, clinical significance, impact on tumor progression, and potential involvement in immune evasion.</p><p><strong>Methods: </strong>UGT1A6 expression across multiple cancer types was analyzed using TNMplot, GEPIA, and The Cancer Genome Atlas (TCGA) databases. Functional experiments, including western blotting, qRT-PCR, CCK-8, and Transwell assays, were performed on pancreatic cancer cell lines to assess their proliferation and migration capabilities. Single-cell data and cell-cell communication analyses using CellChat were conducted to investigate UGT1A6's influence on the immune microenvironment.</p><p><strong>Results: </strong>UGT1A6 expression was significantly upregulated in pancreatic cancer tissues and correlated with poor overall survival (P = 0.0095), advanced TNM stage, and KRAS and TP53 mutations. Functional experiments revealed that UGT1A6 knockdown markedly suppressed the proliferation and migration of pancreatic cancer cells. Immune analysis demonstrated a positive correlation between UGT1A6 and immunosuppressive molecules (CD274, PDCD1LG2, HAVCR2, and TGFBR1) and specific immune cell infiltration patterns, indicating a potential role in promoting immune evasion. Single-cell analysis further showed enhanced communication between UGT1A6-expressing tumor epithelial cells and immune cells, which might impair antitumor immune responses.</p><p><strong>Conclusion: </strong>UGT1A6 acts as a key driver of pancreatic cancer progression and immune evasion, and is emerging as a promising prognostic biomarker and therapeutic target. Future studies should focus on clarifying the detailed molecular mechanisms and validating their clinical utility in precision therapy.</p>","PeriodicalId":50685,"journal":{"name":"Clinical & Translational Oncology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144486821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances in molecular mechanisms of microRNAs in pathogenesis and resistance of treatment in glioblastoma.","authors":"Siddharth Shah, Sai Lavanya Patnala, Mihit Kalawatia, Brandon Lucke-Wold","doi":"10.1007/s12094-025-03969-z","DOIUrl":"https://doi.org/10.1007/s12094-025-03969-z","url":null,"abstract":"<p><p>Glioblastoma (GBM) is the most aggressive brain cancer with poor prognosis, even with current treatments combining surgery, chemotherapy, and radiation. Despite initial tumor removal, recurrence is common and driven by altered genetic profiles. MicroRNAs (miRNAs), small non-coding RNAs with regulatory roles, are implicated in GBM progression through their influence on key hallmarks such as angiogenesis, proliferation, immune evasion, and resistance to therapy. This review systematically analyzed peer-reviewed literature from 2019 to 2025 to evaluate recent findings on miRNAs in GBM pathogenesis. Studies reveal differential miRNA expression in GBM models and their involvement in tumor biology via modulation of target genes. Understanding miRNA networks, along with the tumor microenvironment and immune interactions, may enable the identification of diagnostic and therapeutic biomarkers. Targeting both tumor and associated immune components presents a promising direction for future GBM therapies.</p>","PeriodicalId":50685,"journal":{"name":"Clinical & Translational Oncology","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144477733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}