Seminars in oncology最新文献

{"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}

{"title":"Baicalein and baicalin in cancer therapy: Multifaceted mechanisms, preclinical evidence, and translational challenges","authors":"Xavier Capó ,&nbsp;Rajesh Kumar ,&nbsp;Abhay Prakash Mishra ,&nbsp;Manisha Nigam ,&nbsp;Neti Waranuch ,&nbsp;Miquel Martorell ,&nbsp;Farukh Sharopov ,&nbsp;Daniela Calina ,&nbsp;Dragoș Popa ,&nbsp;William N. Setzer ,&nbsp;Javad Sharifi-Rad ,&nbsp;Raffaele Pezzani","doi":"10.1016/j.seminoncol.2025.152377","DOIUrl":"10.1016/j.seminoncol.2025.152377","url":null,"abstract":"<div><div>Natural compounds with multitargeted actions are gaining prominence in oncology for their potential to complement and transcend the limitations of conventional therapies. Among them, baicalein and baicalin, two flavonoids primarily isolated from <em>Scutellaria baicalensis</em>, have attracted attention for their broad-spectrum anticancer properties. This review synthesizes current evidence from cellular systems, animal models, and early-phase clinical studies, exploring their pharmacological potential and translational relevance. Both molecules interfere with key hallmarks of cancer, including proliferation, survival, angiogenesis, metastasis, and immune evasion. Mechanistically, they modulate interconnected signaling cascades governing apoptosis, inflammation, and cell cycle control, and they enhance tumor sensitivity to chemotherapy and radiotherapy. <em>In-vivo</em> models consistently demonstrate tumor growth inhibition, while clinical data suggest a favorable safety profile, even at relatively high oral doses. However, their clinical translation remains hampered by limited solubility, poor oral bioavailability, and rapid metabolism, factors that continue to constrain their therapeutic window. Efforts to overcome these barriers through structural modification, encapsulation strategies, and advanced delivery systems are underway, yet few have advanced beyond preclinical validation. Despite these pharmacokinetic limitations, baicalein and baicalin remain compelling candidates for integrative oncological approaches. Their pleiotropic mechanisms, combined with low toxicity and synergistic behavior with standard therapies, position them as prototypes for a new generation of phytochemical-based anticancer agents. Continued work is needed to resolve formulation challenges and define precise molecular targets, but their trajectory reflects the growing scientific and clinical momentum around rationally designed natural compound therapeutics.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"Article 152377"},"PeriodicalIF":3.0,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144549944","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":"Breaking barriers: Deciphering the mechanisms of Olaparib resistance in prostate cancer","authors":"Amr Ali Mohammed Abdelgawwad Wl-Sehrawy ,&nbsp;Mahmood Yaseen Mukhlif ,&nbsp;Aysar Ashour Khalaf ,&nbsp;Subasini Uthirapathy ,&nbsp;Suhas Ballal ,&nbsp;Abhayveer Singh ,&nbsp;V. Kavitha ,&nbsp;Laxmidhar Maharana ,&nbsp;Hayder Ridha-Salman ,&nbsp;Ahmed Remthan Hussein Al-Altememe","doi":"10.1016/j.seminoncol.2025.152375","DOIUrl":"10.1016/j.seminoncol.2025.152375","url":null,"abstract":"<div><div>A poly (ADP-ribose) polymerase (PARP) inhibitor, Olaparib has shown notable clinical effectiveness in treating metastatic castration-resistant prostate cancer (mCRPC) with DNA damage repair gene mutations. Though initial reactions were encouraging, the emergence of resistance poses a major clinical problem that reduces the long-term therapeutic value for patients. This paper thoroughly investigates the molecular processes behind acquired and intrinsic resistance to Olaparib in prostate cancer (PCa). Among the several resistance routes discovered are restoration of homologous recombination (HR) repair capacity via secondary BRCA2 mutations, loss of 53BP1/REV7/Shieldin complex activity, and activation of alternative DNA repair pathways. Recent studies further imply that changes in cell cycle checkpoints and epigenetic changes could help to increase therapy resistance even more. Knowing these several resistance mechanisms helps one to create reasonable combination strategies and biomarker-driven initiatives to defeat Olaparib resistance. Among the new treatment options are combination therapies aimed at compensatory DNA repair mechanisms, cell cycle checkpoint inhibitors, epigenetic modulators, and methods tackling tumor microenvironment elements. Predictive biomarker discovery of resistance will help to guide individual treatment choice and sequential therapy optimization, hence changing clinical results for advanced PCa patients in the precision medicine age.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 4","pages":"Article 152375"},"PeriodicalIF":3.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480907","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":"Peripheral blood CD4+CD25+ T lymphocytes and TGF-β predict the prognosis in relapsed/refractory multiple myeloma treated with daratumumab","authors":"Hanyue Xue ,&nbsp;Fang Wei ,&nbsp;Ruiyang Li","doi":"10.1016/j.seminoncol.2025.152373","DOIUrl":"10.1016/j.seminoncol.2025.152373","url":null,"abstract":"<div><div>For patients with relapsed/refractory multiple myeloma (R/RMM), it is indispensable to choose a combination regimen based on Daratumumab, a kind of CD38-targeting monoclonal antibody (mAb), which has prominent therapeutic advantages. However, a few patients still experienced rapid progression, and the predictors of prognosis are little known. Thus, we analyzed peripheral blood (PB) CD4⁺CD25⁺ T lymphocytes and transforming growth factor-β (TGF-β) of R/RMM patients before Daratumumab treatment, to clarify their correlation with survival. Flow cytometry (FCM) was employed to detect, analyze, and compare CD4⁺CD25⁺T lymphocytes. Enzyme-linked immunosorbent assay (ELISA) was utilized to quantify serum TGF-β. Clinical indicators were gathered and classified into quartiles. In R/RMM patients’ PB, we compared these markers between the upper and lower three quartiles. We found that CD4⁺CD25⁺ T lymphocytes (pcs/µL) and TGF-β in the PB of the R/RMM patients were higher than those of the newly diagnosed MM (NDMM) patients. Additionally, serum TGF-β of R/RMM patients was positively correlated to serum creatinine (Scr) (<em>P</em> &lt; 0.05). Finally, high CD4⁺CD25⁺ T lymphocytes (pcs/µL, 95% confidence interval [CI], 4.312–7.028, <em>P</em> = 0.001), CD4⁺CD25⁺ T lymphocytes (%, median PFS: 5.67 months, <em>P</em> = 0.043), and Scr (µmol/l, 95% CI, 5.378–7.422, <em>P</em> = 0.005) of R/RMM patients were significantly associated with inferior progression-free survival (PFS). These results suggest that patients with R/RMM are rich in CD4⁺CD25⁺ T lymphocytes and TGF-β. Additionally, R/RMM patients with elevated CD4⁺CD25⁺ T lymphocytes, TGF-β, and Scr before the treatment of daratumumab are more likely to have a poor prognosis.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 4","pages":"Article 152373"},"PeriodicalIF":3.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480909","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":"Are we there yet? Gut microbiota for cancer diagnosis, prognosis and treatment","authors":"Carlos Ordóñez ,&nbsp;Sara Zurita ,&nbsp;Giuliana Ramírez ,&nbsp;Fernanda Cordeiro ,&nbsp;Katherine Garcia-Matamoros ,&nbsp;Fuad Huaman-Garaicoa ,&nbsp;Andrea Orellana-Manzano ,&nbsp;Lorena Sandoya-Onofre ,&nbsp;Juan Pogo ,&nbsp;Diana Carvajal-Aldaz","doi":"10.1016/j.seminoncol.2025.152376","DOIUrl":"10.1016/j.seminoncol.2025.152376","url":null,"abstract":"<div><div>Cancer remains as one of the leading causes of death worldwide, emphasizing the need for innovative diagnostic and therapeutic tools. The gut microbiota has emerged as a factor that influences cancer progression, prognosis, and treatment outcomes. This review analyzes observational and interventional studies conducted with human subjects over the past 5 years, highlighting significant advancements in gut microbiota research for cancer management. Observational studies consistently demonstrated differences in gut microbial composition between cancer patients and healthy controls. Moreover, microbial diversity, particularly at the species and strain level, correlated significantly with clinical outcomes. Interventional studies showed the potential of probiotics and fecal microbiota transplantation (FMT) as adjuncts in cancer therapy by restoring microbial diversity, reducing inflammation, and alleviating chemotherapy-induced complications. Collectively, these findings suggest the gut microbiota’s potential as a tool for cancer care. Future research should focus on standardizing taxonomic-level analyses, optimizing probiotic formulations, and validating FMT/AFMT clinical protocols to fully harness the gut microbiota’s diagnostic and therapeutic capabilities in oncology.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 4","pages":"Article 152376"},"PeriodicalIF":3.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472024","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}