Seminars in oncology最新文献

{"title":"Lactylation in radiosensitivity regulation: Mechanistic insights and recent advances","authors":"Caiqiang Zhu ,&nbsp;Meng Tian ,&nbsp;Xiaoke Di ,&nbsp;Jin Liu ,&nbsp;Huanhuan Chen ,&nbsp;Lu Xu ,&nbsp;Ying Liu ,&nbsp;Xinchen Sun ,&nbsp;Zhaoyue Zhang","doi":"10.1016/j.seminoncol.2025.152394","DOIUrl":"10.1016/j.seminoncol.2025.152394","url":null,"abstract":"<div><div>Lactylation, as a novel post-translational modification, has gained a lot of attention in the biomedical field in recent years. Lactylation is not only related to cellular metabolism but also increasingly prominent in the tumor microenvironment, particularly in regulating radiation sensitivity. This review aims to explore the potential connection between lactylation modification and the regulation of radiation sensitivity. Current research shows that lactylation might be crucial in how tumor cells respond to radiotherapy by influencing energy metabolism, gene expression, and cell signaling. However, despite preliminary studies revealing the association between lactylation and radiation sensitivity, the understanding of its specific mechanisms remains insufficient, necessitating more systematic research to elucidate this process. Therefore, by analyzing the biological basis of lactylation modification, its role in tumor metabolism, and its relationship with radiotherapy, we summarize the importance and application prospects of lactylation in tumor treatment, providing direction for future research.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"Article 152394"},"PeriodicalIF":3.0,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144712849","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":"Germline mutations in B-cell non-Hodgkin lymphoma-associated hemophagocytic lymphohistiocytosis (LA-HLH) and patient outcomes","authors":"Xing Zhong ,&nbsp;Xinyu Zhu ,&nbsp;Xiaoxia Ma ,&nbsp;Lili Zhou ,&nbsp;Xiu Luo ,&nbsp;Ping Li ,&nbsp;Yi Ding ,&nbsp;Jianfei Fu ,&nbsp;Jiaqi Bo ,&nbsp;Muye Yang ,&nbsp;Aibin Liang ,&nbsp;Yu Zeng ,&nbsp;Bing Xiu","doi":"10.1016/j.seminoncol.2025.152388","DOIUrl":"10.1016/j.seminoncol.2025.152388","url":null,"abstract":"<div><div>Lymphoma-associated hemophagocytic lymphohistiocytosis/syndrome (LA-HLH/LAHS) represents the most prevalent form of malignancy-associated HLH and is associated with an exceptionally poor prognosis. Emerging evidence implicates germline mutations as potential contributors to hematologic abnormalities, suggesting a genetic predisposition in affected individuals.</div><div>We conducted whole-exome sequencing (WES) on a cohort of 12 LA-HLH patients, with detailed analysis of 3 representative cases exhibiting coexisting genetic disorders. These cases were comprehensively evaluated for their clinical management strategies and therapeutic outcomes.</div><div>Our study revealed that gene mutations were detected in 6 patients (6/12), including 2 had somatic mutations, 3 had germline mutations, and 1 had both somatic and germline mutations. Among the 4 patients harbored germline mutations, 3 were diagnosed with concurrent genetic disease. Most patients (11/12) responded to immunochemotherapy for a short time and then progressed or relapsed, even after autologous hematopoietic stem cell transplantation (ASCT). Interestingly, two patients received CAR-T-cell therapy and achieved extremely good responses. One patient received CD19 CAR-T-cell infusion and had a PFS of 26 months. The other patient received double CAR-T infusions and has remained in complete remission for more than 2 years (until now).</div><div>This study proposes that LA-HLH may constitute a novel genetic subtype of lymphoma. Systematic genetic sequencing should be prioritized to guide precision treatment approaches in selected cases, including immunotherapies such as CAR-T-cell therapy. These insights redefine our understanding of LA-HLH pathogenesis and clinical intervention strategies.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"Article 152388"},"PeriodicalIF":3.0,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144679765","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":"Deciphering the prognostic value and immunotherapeutic strategy of aggrephagy in melanoma: Integrating single-cell sequencing and machine learning","authors":"Zihao Li ,&nbsp;Jiaheng Xie ,&nbsp;Liqun Li ,&nbsp;Yucang He ,&nbsp;Wanying Chen ,&nbsp;Hao Dai ,&nbsp;Songyun Zhao","doi":"10.1016/j.seminoncol.2025.152371","DOIUrl":"10.1016/j.seminoncol.2025.152371","url":null,"abstract":"<div><div>This study aimed to investigate the role of aggrephagy in cutaneous melanoma (CM) and explore its potential as a biomarker for prognosis and therapeutic targeting. We utilized single-cell sequencing technology and machine learning algorithms to analyze melanoma transcriptome data from the TCGA database and validated our findings using 3 independent datasets from the GEO database. By employing enrichment scoring in single-cell sequencing, we identified characteristic expression patterns of different cell types involved in aggrephagy and constructed an aggrephagy-related signature (ARS). We further evaluated the association of ARS with clinical features, immune cell infiltration, tumor mutational load (TMB), and immune checkpoint gene expression. Additionally, we conducted in vivo experiments by knocking down TPX2, the most critical oncogene in ARS, using shRNA and assessed its effects on tumor proliferation and T-cell growth via subcutaneous tumor formation assays and flow cytometry in mice. The ARS demonstrated robust prognostic predictive power across multiple datasets, with higher ARS scores associated with poorer overall survival (OS) and lower levels of immune cell infiltration. Patients with low ARS scores were more likely to benefit from immune checkpoint inhibitor therapies, while those with high scores exhibited increased sensitivity to 2 common chemotherapeutic agents. Compared to published melanoma prognostic models, our ARS showed higher accuracy and stability. The construction of an ARS-related nomogram further facilitated more accurate clinical decision-making. In vivo experiments confirmed that TPX2 knockdown inhibited tumor proliferation and enhanced T-cell growth, highlighting its critical role in CM progression. Our study highlights the complex functions of the aggrephagy-related signature in cutaneous melanoma, underscoring its potential as a therapeutic target and a valuable tool for prognostic assessment.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"Article 152371"},"PeriodicalIF":3.0,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144670408","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":"Prostate cancer in Türkiye: Trend analysis of incidence and mortality rates","authors":"Guven Turan ,&nbsp;Merve Turan ,&nbsp;Yasemin Basbinar ,&nbsp;Hulya Ellidokuz","doi":"10.1016/j.seminoncol.2025.152391","DOIUrl":"10.1016/j.seminoncol.2025.152391","url":null,"abstract":"<div><div>Prostate cancer is a significant global health concern, with substantial regional variations in incidence and mortality rates. In Türkiye, it's the second most common cancer and fourth leading cause of cancer-related deaths among men. This study aims to analyze trends in prostate cancer incidence and mortality rates in Türkiye. Prostate cancer trends in Türkiye is analyzed by using data of incidence from Türkiye Cancer Statistics Reports and mortality from TurkStat. Trends in incidence and mortality rates were analyzed using Joinpoint regression, evaluating average annual percentage changes and annual percentage change (APC). From 2004 to 2018, age-standardized prostate cancer incidence rate increased from 24.9 to 40.3 per 100,000, with the highest in aged 75 and older. The Annual Average Percentage Change (AAPC) was 2.6%[CI, 1.1 to 4.3] overall, with specific rates of 2.3% [CI, 0.5 to 3.5] in the 50–54 and −1.9% [CI, −3.7 to −0.1] in the 80–84 age group. The APC was 9.2% [CI, 3.6 to 24.8] from 2004 to 2008. From 2016–2018, APCs in 50–54 and 60–64 age groups are 13.4% [CI, 3.6 to 20.4] and 13.7% [CI, 0.4 to 23.6], respectively. Mortality rate ranged from 7.3 to 9.2 per 100,000 from 2009 to 2022, with a 4.9% [CI, 2.1 to 11.6] increase in 2009–2014 and a 1.9%–1.9%[CI, 4.4 to −0.6] decrease in 2014–2022. The incidence rate of prostate cancer in Türkiye increased until 2008, but then stabilised with the rates rising at the age of 50–54 and decreasing at the age of 80–84 years. Mortality rates initially increased but declined in the last 8 years. Further research is needed to explore factors influencing these trends.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"Article 152391"},"PeriodicalIF":3.0,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144665963","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":"Clinical efficacy and security analysis of DEB-TACE combined with trans arterial infusion of carrelizumab in the therapy of advanced liver cancer","authors":"Yang Chen,&nbsp;Xinxin Zang,&nbsp;Xiaoxuan Zhang,&nbsp;Songyan Zhang","doi":"10.1016/j.seminoncol.2025.152393","DOIUrl":"10.1016/j.seminoncol.2025.152393","url":null,"abstract":"<div><div>To explore the clinical efficacy and security analysis of DEB-TACE combined with carrelizumab in the therapy of advanced liver cancer. This study was prospectively designed. Using a random number table method, 96 patients with advanced liver cancer hospitalized from August 2022 to August 2023 were divided into the DT group (DEB-TACE treatment, <em>n</em> = 48) and the DT-C group (on the basis of the DT group, receiving carrelizumab infusion via hepatic artery, <em>n</em> = 48). The changes of therapeutic effect, serum tumor markers, T lymphocyte subsets, overall survival (OS) and progression-free survival (PFS) and the adverse effect were observed. The ORR and DCR of the DT-C group were higher than that of the DT group (<em>P</em> &lt; 0.05). After 1 month of treatment, CD3⁺, CD4⁺ and CD4⁺/CD8⁺ were increased and the DT-C group was higher than the DT group (<em>P</em> &lt; 0.001). The CD8+ decreased after 1 month of treatment, and the CD8+ in the DT-C group was significantly lower than that in the DT group (<em>P</em> &lt; 0.001). AFP and PIVKA-II decreased after 1 month of treatment, and the DT-C group was lower than the DT group (<em>P</em> &lt; 0.001). The overall survival (OS) (2-year survival rate 33.33%) and progression-free survival (PFS) (2-year survival rate 18.75%) of the DT-C group were higher than those of the DT group (<em>P</em> &lt; 0.05). There was no difference in the adverse reaction incidence (<em>P</em> &gt; 0.05). DEB-TACE combined with trans arterial infusion of carrelizumab is safe and effective in the treatment of advanced liver cancer. Compared with DEB-TACE alone, this combination therapy results in higher CD3+, CD4+, and CD4+/CD8+ levels, as well as reduced CD8+, AFP, and PIVKA-II levels.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"Article 152393"},"PeriodicalIF":3.0,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144657305","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":"Metabolic reprogramming: The driving force behind cancer drug resistance","authors":"Amr Ali Mohamed Abdelgawwad El-Sehrawy ,&nbsp;Chou-Yi Hsu ,&nbsp;Ali G. Alkhathami ,&nbsp;Muktesh Chandra ,&nbsp;Tina Saeed Basunduwah ,&nbsp;H. Malathi ,&nbsp;Jitendra Narayan Senapati ,&nbsp;Apurav Gautam ,&nbsp;Mundher Kadhem ,&nbsp;Hatif Abdulrazaq Yasin","doi":"10.1016/j.seminoncol.2025.152392","DOIUrl":"10.1016/j.seminoncol.2025.152392","url":null,"abstract":"<div><div>Metabolic reprogramming enables stress adaptation of cancer cells to treatment and is a primary causative force of drug resistance. Dysregulation of glucose, amino acid, and lipid metabolism supplies energy, biosynthetic precursors, and redox balance, promoting survival in the treated tumor. These processes are coordinated by oncogenic signaling, loss of tumor suppressors, and regulatory non-coding RNAs, which promote cancer stemness, immune evasion, and resistance to apoptosis. This review examines the mechanisms by which central metabolic pathways, particularly glycolysis, glutamine metabolism, and fatty acid synthesis, are altered to facilitate drug resistance in various types of cancer. Additionally, we report on novel therapeutic approaches that exploit such metabolic weaknesses to prevent therapy resistance and enhance clinical outcomes. Future directions emphasize the need for advanced metabolic profiling to personalize treatment approaches and the clinical translation of promising preclinical findings to overcome this significant obstacle in cancer therapy.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"Article 152392"},"PeriodicalIF":3.0,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144634120","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":"From tissue architecture to clinical insights: Spatial transcriptomics in solid tumor studies","authors":"Arpit Sharma ,&nbsp;Shruti S. Raut ,&nbsp;Alok Shukla ,&nbsp;Shivani Gupta ,&nbsp;Abha Mishra ,&nbsp;Amit Singh","doi":"10.1016/j.seminoncol.2025.152389","DOIUrl":"10.1016/j.seminoncol.2025.152389","url":null,"abstract":"<div><div>Cancer is a highly heterogeneous disease, and its diagnosis, prognosis, and therapeutic responsiveness depend not only on genetic alterations but also on the intricate organization of cells within the tumor microenvironment (TME). Spatial transcriptomics—a suite of techniques that preserves the spatial context of gene expression in intact tissue—has revolutionized our ability to decipher tumor architecture and intercellular communication. This review provides an in‐depth analysis of recent advancements in spatial transcriptomics technologies and their applications in solid tumor research. We first describe the evolution of spatial transcriptomics from early in situ hybridization methods to state‐of‐the‐art imaging‐ and sequencing‐based platforms. Next, we discuss how spatially resolved transcriptomics is transforming cancer research by revealing the molecular landscapes of tumor cores, invasive edges, and immunological niches. The integration of spatial transcriptomics with single‐cell multiomics and advanced computational algorithms is leading to the identification of novel prognostic and predictive biomarkers. Despite tremendous progress, challenges remain in terms of technical resolution, data processing, sample preparation, and clinical standardization. Finally, we highlight emerging trends—including three-dimensional (3D) spatial profiling, multimodal integration, and the use of artificial intelligence and Deep learning—to envision a future in which spatial transcriptomics will serve as a pivotal tool for precision oncology. Together, these developments promise to refine cancer biomarker studies and ultimately improve patient outcomes.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"Article 152389"},"PeriodicalIF":3.0,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144631889","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":"Multiple myeloma: Insights into underlying mechanisms, advances in diagnostic and therapeutic modalities","authors":"Rohitash Yadav ,&nbsp;Jitendra Kumar Chaudary ,&nbsp;Khushboo Bisht ,&nbsp;Puneet Dhamija ,&nbsp;Pankaj Kumar Chaudhary ,&nbsp;Uttam Kumar Nath ,&nbsp;Neeraj Jain","doi":"10.1016/j.seminoncol.2025.152390","DOIUrl":"10.1016/j.seminoncol.2025.152390","url":null,"abstract":"<div><div>Multiple myeloma (MM) is characterized by malignant proliferation and accumulation of terminally differentiated antibody-producing plasma cells in bone marrow. The underlying genetic causes of MM are highly complex, involving the loss of function in a myriad of crucial genes, especially those involved in DNA replication fidelity and repair. The important genetic events underscoring MM mutagenesis entail large-scale chromosomal aberrations, localized genetic changes, defective DNA repair mechanisms, point mutation, and mutagenic activity of enzymes such as activation-induced deaminase (AID) and apolipoprotein B mRNA editing enzyme, and catalytic polypeptide (APOBEC). Despite considerable improvement in treatment regimen, MM disease remains incurable for majority of patients with very high mortality. Notably, delay in diagnosis of MM could indirectly contribute to the worse clinical outcomes and lower treatment responsiveness through several mechanisms. Primarily, MM diagnosis relies on histopathological changes and molecular profiling of the patient’s sample. In the past decades, new methods of MM diagnosis and therapeutic approaches have been invented. Together, advances in disease understanding, diagnosis, and novel effective therapeutic interventions have substantially helped slow down and/or arresting the disease progression in the large number of patients, thereby increasing overall survival. This review discusses the genetic causes of MM, clinical presentation, advances in diagnosis, and new therapeutic interventions, including combinations of effective agents targeting relapse/refractory MM.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"Article 152390"},"PeriodicalIF":3.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144597079","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":"LncRNA THUMPD3-AS1 promotes the proliferation and migration of esophageal cancer cells through the miR-29a-3p/ELK1/PRDX4 signaling pathway","authors":"Mingming Tang ,&nbsp;Jianjun Sun ,&nbsp;Zhigang Cai","doi":"10.1016/j.seminoncol.2025.152350","DOIUrl":"10.1016/j.seminoncol.2025.152350","url":null,"abstract":"<div><div>Esophageal cancer (ESCA) is a significant contributor to cancer-related deaths worldwide due to its aggressive nature and poor prognosis. Recent research indicates that non-coding RNAs are critical in tumor progression. This study intends to explore the interaction between LncRNA THUMPD3-AS1 and miR-29a-3p in ESCA advancement. By conducting bioinformatic analyses and validating differentially expressed genes in ESCA clinical samples, the regulatory relationship between THUMPD3-AS1, miR-29a-3p, ETS transcription factor (ELK1), and Peroxiredoxin 4 (PRDX4) was investigated using various functional assays. In vitro and in vivo experiments were also carried out to assess the impact of this interaction on tumor growth and ESCA progression. Results indicated elevated levels of THUMPD3-AS1 in ESCA tissues, acting as a sponge for miR-29a-3p, a microRNA known for its tumor-suppressive properties. This interaction relieved miR-29a-3p's inhibition of ELK1, resulting in increased PRDX4 expression. Functional tests confirmed that the THUMPD3-AS1/miR-29a-3p/ELK1/PRDX4 axis supports tumor proliferation, migration, and invasion in ESCA. Further validation of these findings was done through in vivo experiments. In conclusion, this study underscores the significance of the THUMPD3-AS1/miR-29a-3p/ELK1/PRDX4 axis as a crucial regulatory pathway in ESCA, unveiling its oncogenic role in enhancing tumor aggressiveness.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 4","pages":"Article 152350"},"PeriodicalIF":3.0,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144579729","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":"MicroRNAs: From bench to bedside applications as breast cancer therapsseutics","authors":"Md Abdus Samad ,&nbsp;Iftikhar Ahmad ,&nbsp;Muhammad Nadeem Asghar ,&nbsp;Mohd Suhail ,&nbsp;Mohd Rehan ,&nbsp;Fahad A. Al-Abbasi ,&nbsp;Khadeejah Alsolami ,&nbsp;Mohd Suhail Akhter ,&nbsp;Ausaf Ahmad ,&nbsp;Shams Tabrez","doi":"10.1016/j.seminoncol.2025.152386","DOIUrl":"10.1016/j.seminoncol.2025.152386","url":null,"abstract":"<div><div>MicroRNAs (miRNAs) or small noncoding RNA molecules, 18–22 nucleotides long, are evolutionarily conserved and may have an impact on the behavior and progression of tumors. Cancer initiation, proliferation, invasion, and metastasis are all related to the specific deregulation of miRNAs. It also affects the genes involved in metabolism, apoptosis, cellular differentiation, and proliferation. Understanding the functional roles of miRNAs could shed light on the intricate molecular mechanism that underlie cancer growth. The purpose of this review is to investigate the presence of tumor-suppressive, oncogenic, and metastatic miRNAs in cancer cells, specifically breast cancer (BC) and how these miRNAs affect the development of BC and its subtypes. In addition, the miRNA-based therapeutic strategies and utilization of different delivery system to enhance the efficacy has also been covered. Based on our article, miRNAs appear to be cutting-edge prognostic, therapeutic, and diagnostic tools for the treatment of BC. However, several barriers, such as, delivery systems, side effects, demographic variabilities, and lengthy clinical studies needs to be optimized before these miRNAs could be routinely used in clinical settings.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"Article 152386"},"PeriodicalIF":3.0,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144550081","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}