Medical Oncology最新文献

{"title":"Three-dimensional in vitro models in head and neck cancer: current trends and applications.","authors":"Masoumeh Amiri, Tayebeh Sadat Tabatabai, Zahra Seifi, Gelavizh Rostaminasab, Abdolhamid Mikaeili, Fatemeh Hosseini, Leila Rezakhani","doi":"10.1007/s12032-025-02737-x","DOIUrl":"10.1007/s12032-025-02737-x","url":null,"abstract":"<p><p>Head and neck cancer (HNC) is the sixth most prevalent malignancy worldwide and includes a variety of upper gastrointestinal abnormalities. HNC includes oral, throat, voice box, nasal cavity, paranasal sinuses, and salivary gland cancers. Squamous cells in the mouth, nose, and throat cause HNC. Drugs, alcohol, poor diets, smoking, and genetics all contribute to this condition. Cancer research has focused on three-dimensional (3D) models in HNC biology in recent decades. An adequate microenvironmental system and cancer cell culture are the initial steps to understanding cancer cells' complicated interactions with their surroundings. New 3D models claim to bridge in vivo and in vitro investigations and erase the gap. Interdisciplinary cell biology and tissue engineering researchers are creating 3D cancer tissue models to better understand the illness and develop more accurate cancer medicines. Tissue engineering researchers, who are always exploring novel approaches to treat cancer, have been able to include the third dimension into laboratory settings and mimic cell-to-cell and cell-to-matrix interactions by recreating the tumor microenvironment using 3D models and so make research on cancer easier. This review addresses recent developments in tissue engineering with an emphasis on 3D models in HNC.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"194"},"PeriodicalIF":2.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144008443","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":"A novel L-shaped ortho-quinone analog targeting adenosine A2b receptor to inhibit epithelial-mesenchymal transition in colorectal cancer cells.","authors":"Rui Wang, Xingsheng Yao, Jia Yu, Xinwei Wan, Shengyou Li, Yuxuan Tian, Guangyang Liu, Ziqi Yang, Xianhui Yang, Sha Cheng, Weidong Pan, Ying Cao, Heng Luo","doi":"10.1007/s12032-025-02767-5","DOIUrl":"10.1007/s12032-025-02767-5","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a common malignancy of the gastrointestinal tract, with its incidence and mortality rates rising significantly in recent decades. In this study, we identified a compound (TC4) from a series of L-shaped ortho-quinone analog with notable inhibitory effects on epithelial-mesenchymal transition (EMT) in CRC cells. In vitro studies demonstrated that TC4 induces apoptosis, thereby suppressing CRC cell growth, invasion, and metastasis. Target analysis suggested that adenosine A2b receptor (ADORA2B) is a key molecular target of TC4, which was further confirmed by thermodynamic experiments showing direct binding to ADORA2B in living cells. Using ADORA2B overexpression and knockdown models, we found that abnormal expression of ADORA2B significantly affects CRC cell growth, invasion, metastasis, and sensitivity to TC4, confirming ADORA2B as a critical target for the compound's anti-tumor activity. TC4 was shown to markedly influence EMT, downregulating E-cadherin while upregulating N-cadherin, Vimentin, and Snail, with these effects dependent on ADORA2B overexpression. This indicates that the regulation of EMT by TC4 is closely associated with its interaction with ADORA2B. The present study confirms that TC4, a newly discovered compound with the ability to inhibit the growth and metastasis of CRC cells, can target ADORA2B to significantly regulate EMT in cancer cells.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"197"},"PeriodicalIF":2.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028756","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":"The gastrointestinal mycobiome in inflammation and cancer: unraveling fungal dysbiosis, pathogenesis, and therapeutic potential.","authors":"Neelakanta Sarvashiva Kiran, Ankita Chatterjee, Chandrashekar Yashaswini, Rohitas Deshmukh, Omar Awad Alsaidan, Sankha Bhattacharya, Bhupendra G Prajapati","doi":"10.1007/s12032-025-02761-x","DOIUrl":"10.1007/s12032-025-02761-x","url":null,"abstract":"<p><p>The gastrointestinal mycobiome, comprising diverse fungal species, plays a significant role in gastrointestinal carcinogenesis and inflammatory bowel disease (IBD) pathogenesis. Recent studies have demonstrated that dysbiosis of the gut mycobiome, characterized by an overrepresentation of pathogenic fungi such as Candida albicans and Aspergillus, correlates with increased inflammation and cancer risk. For instance, C. albicans has been shown to induce colonic inflammation through the activation of pattern recognition receptors and the release of pro-inflammatory cytokines, exacerbating IBD symptoms and potentially facilitating tumorigenesis. Additionally, metagenomic analyses have revealed distinct fungal signatures in colorectal cancer tissues compared to adjacent healthy tissues, highlighting the potential of fungi as biomarkers for disease progression. Mechanistically, gut fungi contribute to disease through biofilm formation, mycotoxin secretion (e.g., aflatoxins, candidalysin), pro-inflammatory cytokine induction (e.g., IL-1β, IL-17), and disruption of epithelial barriers-creating a tumor-promoting and inflammation-prone environment. Furthermore, the interplay between fungi and the bacterial microbiome can amplify inflammatory responses, contributing to chronic inflammation and cancer development. Fungal interactions with bacterial communities also play a synergistic role in shaping mucosal immune responses and enhancing disease severity in both cancer and IBD contexts. As research continues to elucidate these complex fungal-host and fungal-bacterial interactions, targeting the gut mycobiome may offer novel therapeutic avenues for managing IBD and gastrointestinal cancers, emphasizing the need for integrated, mechanistically informed approaches to microbiome research.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"195"},"PeriodicalIF":2.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144027729","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":"Targeting exon mutations in NSCLC: clinical insights into LAG-3, TIM-3 pathways, and advances in fourth-generation EGFR-TKIs.","authors":"Koteeswaran Kannan, Sumithra Mohan","doi":"10.1007/s12032-025-02755-9","DOIUrl":"10.1007/s12032-025-02755-9","url":null,"abstract":"<p><p>Lung cancer remains the second leading cause of cancer-related morbidity and mortality worldwide, with non-small cell lung cancer (NSCLC) accounting for the majority of cases. Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have become the standard first-line therapy for advanced NSCLC with EGFR mutations, offering significant improvements in progression-free survival (PFS), overall survival (OS), and objective response rate (ORR) compared to chemotherapy alone. Recent studies suggest that their effectiveness decreased with the emergence of acquired resistance, such as C797S and T790M. Immunotherapy alone also shows enhanced PFS and OS over chemotherapy; however, its applicability can be limited in cases with low programmed cell death ligand 1 (PD-L1) expression and result in immune-related adverse effects like those observed in retrospective, non-randomized studies. Emerging fourth-generation EGFR-TKIs, currently under clinical trials, show promising potential to address these resistance mechanisms. Advanced inhibitors, including BBT-176, BLU-945, and BLU-701, have effectively targeted resistant mutations and reduced disease progression. Studies have suggested that combining fourth-generation EGFR-TKIs with immunotherapies targeting novel pathways like LAG-3 and TIM-3 may enhance patient outcomes. Such combination regimens aim to optimize PFS, OS, and ORR while minimizing adverse effects and addressing the limitations of current therapies. This study explores the landscape of EGFR mutations, their clinical significance, and the integration of innovative fourth-generation EGFR-TKIs with immunotherapies, emphasizing the potential of precision medicine in advancing the management of EGFR-mutated NSCLC.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"196"},"PeriodicalIF":2.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144022217","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":"Exosomal miRNA-based theranostics in cervical cancer: bridging diagnostics and therapy.","authors":"Neha R Raghani, Mehul R Chorawala, Kavya Parekh, Anvesha Sharma, Omar Awad Alsaidan, Prawez Alam, Mohammad Fareed, Bhupendra Prajapati","doi":"10.1007/s12032-025-02752-y","DOIUrl":"10.1007/s12032-025-02752-y","url":null,"abstract":"<p><p>Cervical cancer (CC) remains a significant global health burden, particularly in low- and middle-income countries, where access to effective screening and treatment is limited. Despite advancements in conventional therapies, such as surgery, chemotherapy, and radiotherapy, challenges related to late-stage diagnosis, treatment resistance, and disease recurrence persist. The emergence of microRNAs (miRNAs) as key regulators of gene expression has revolutionized cancer diagnostics and therapeutics. Exosomal miRNAs, in particular, have garnered attention due to their stability, detectability in bodily fluids, and pivotal roles in tumor progression, metastasis, and immune modulation. This review provides a comprehensive overview of the role of exosomal miRNAs in the theranostic landscape of CC. We explore their involvement in disease pathogenesis, highlighting their potential as minimally invasive diagnostic biomarkers for early detection and disease monitoring. Furthermore, we examine their utility in therapeutic strategies, including miRNA-mediated drug delivery systems and miRNA-targeted interventions to overcome chemoresistance. Integrating exosomal miRNA profiling with current diagnostic modalities could enhance screening sensitivity and specificity, while miRNA-based therapies offer novel avenues to improve treatment efficacy. This review discusses recent advancements in miRNA research, current challenges in clinical translation, and future perspectives on leveraging exosomal miRNAs for personalized CC care.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"193"},"PeriodicalIF":2.8,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144016457","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":"Unraveling the mechanisms of tricetin in renal cell carcinoma treatment through network pharmacology and experimental validation.","authors":"Kai Meng, Zixuan Chen, Yu Zhang, Xingyu Chen, Taoying Chen, Ya Song, Xing Jia, Min Liu","doi":"10.1007/s12032-025-02744-y","DOIUrl":"10.1007/s12032-025-02744-y","url":null,"abstract":"<p><p>Renal cell carcinoma (RCC), one of the most common types of kidney cancer, represents a major global health concern due to its increasing incidence and high death rates. While conventional treatment modalities have improved patient outcomes, they often face limitations such as drug resistance, severe adverse effects, and limited efficacy in advanced or metastatic cases. These challenges highlight the urgent need for novel therapeutic approaches to enhance RCC management. Tricetin, a natural flavonoid abundant in cereal plants, has shown promising anticancer activity in various malignancies by inhibiting cancer cell proliferation, migration, and invasion. However, the molecular mechanisms underlying Tricetin's effects on RCC remain poorly understood. In this research, we employed network pharmacology to identify key molecular targets of Tricetin in RCC and evaluated its binding affinity to these targets using molecular docking techniques. Bioinformatics analyses were conducted to predict the potential biological pathways involved. Furthermore, in vitro experiments using RCC cell lines (786-O and ACHN) demonstrated that Tricetin suppresses cell proliferation and migration, likely through modulation of the EGFR/PI3K/Akt signaling pathway. Overall, our findings offer new insights into the therapeutic potential of Tricetin and provide a foundation for developing targeted treatment strategies to improve RCC outcomes.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"192"},"PeriodicalIF":2.8,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989679","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":"Deciphering the role of circular RNAs in cancer progression under hypoxic conditions.","authors":"Hamza Abu Owida, Raed Obaid Saleh, Suleiman Ibrahim Mohammad, Asokan Vasudevan, R Roopashree, Aditya Kashyap, Anima Nanda, Subhashree Ray, Ahmed Hussein, Hatif Abdulrazaq Yasin","doi":"10.1007/s12032-025-02727-z","DOIUrl":"10.1007/s12032-025-02727-z","url":null,"abstract":"<p><p>Hypoxia, characterized by reduced oxygen levels, plays a pivotal role in cancer progression, profoundly influencing tumor behavior and therapeutic responses. A hallmark of solid tumors, hypoxia drives significant metabolic adaptations in cancer cells, primarily mediated by hypoxia-inducible factor-1α (HIF-1α), a key transcription factor activated in low-oxygen conditions. This hypoxic environment promotes epithelial-mesenchymal transition (EMT), enhancing cancer cell migration, metastasis, and the development of cancer stem cell-like properties, which contribute to therapy resistance. Moreover, hypoxia modulates the expression of circular RNAs (circRNAs), leading to their accumulation in the tumor microenvironment. These hypoxia-responsive circRNAs regulate gene expression and cellular processes critical for cancer progression, making them promising candidates for diagnostic and prognostic biomarkers in various cancers. This review delves into the intricate interplay between hypoxic circRNAs, microRNAs, and RNA-binding proteins, emphasizing their role as molecular sponges that modulate gene expression and signaling pathways involved in cell proliferation, apoptosis, and metastasis. It also explores the relationship between circRNAs and the tumor microenvironment, particularly how hypoxia influences their expression and functional dynamics. Additionally, the review highlights the potential of circRNAs as diagnostic and prognostic tools, as well as their therapeutic applications in innovative cancer treatments. By consolidating current knowledge, this review underscores the critical role of circRNAs in cancer biology and paves the way for future research aimed at harnessing their unique properties for clinical advancements. Specifically, this review examines the biogenesis, expression patterns, and mechanistic actions of hypoxic circRNAs, focusing on their ability to act as molecular sponges for microRNAs and their interactions with RNA-binding proteins. These interactions impact key signaling pathways related to tumor growth, metastasis, and drug resistance, offering new insights into the complex regulatory networks governed by circRNAs under hypoxic stress.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"191"},"PeriodicalIF":2.8,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144021497","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":"The evolving landscape of oncolytic virus immunotherapy: combinatorial strategies and novel engineering approaches.","authors":"Mujibullah Sheikh, Arshiya Saiyyad, Aimé Aliunui, Pranita S Jirvankar","doi":"10.1007/s12032-025-02746-w","DOIUrl":"10.1007/s12032-025-02746-w","url":null,"abstract":"<p><p>Oncolytic viruses (OVs) are a promising class of cancer therapy, exploiting their abilities to selectively infect and kill cancer cells while stimulating antitumor immune responses. The current assessment explores the changing horizons of OV immunotherapy, focusing on recent advances in technology plans to improve OV projects and combined approaches to improve curative efficacy. We discuss how OVs induce direct oncolysis and promote the release of tumor-associated antigens, leading to the activation of both innate and adaptive immunity. Special attention shall be given to programs for arm OVs to express curative genes, modify the tumor microenvironment and overcome immunosuppression. Moreover, we assess the synergies of uniting OVs with other immunotherapeutic techniques, such as immune checkpoint inhibitors and cell therapy, to improve tolerant outcomes. The present assessment provides an understanding of the relevant declaration of the OV analysis, highlighting the main obstacles and the future directions for the development of other capable and targeted cancer immunotherapy.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"190"},"PeriodicalIF":2.8,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144044013","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":"Ursolic acid induces apoptosis in nasopharyngeal carcinoma cells through the P53 signaling pathway: a network pharmacology and experimental validation study.","authors":"Binya Wang, Keying Huang, Jiale Xiao, Yangyang Tao, Jingjing Luo, Yonghui Wu, Sainan Zhou, Yingchun He, Lan He","doi":"10.1007/s12032-025-02749-7","DOIUrl":"10.1007/s12032-025-02749-7","url":null,"abstract":"<p><p>Nasopharyngeal carcinoma (NPC) is a malignant neoplasm that is highly prevalent in East Asia and presents significant therapeutic challenges due to limited treatment options and severe adverse effects. Ursolic acid (UA) is a pentacyclic triterpenoid with anticancer activity in various tumors; however, its mechanism of action in NPC remains unclear. This study integrated network pharmacology with experimental validation to elucidate the molecular mechanism underlying the effect of UA against NPC. Screening of a network pharmacology database identified 39 targets common to UA and NPC, among which P53, STAT3, Bcl-2, IL1B, and CASP3 showed high node degrees in the protein-protein interaction network. Gene Ontology analysis revealed that these targets were primarily enriched in stress response and apoptosis regulation, whereas Kyoto Encyclopedia of Genes and Genomes analysis indicated significant enrichment in the P53 signaling and apoptosis pathways. UA dose-dependently inhibited the proliferation of the NPC cell lines S18 and S26 (p < 0.01), and induced apoptosis, as demonstrated by Annexin V-FITC/PI double fluorescence staining and confirmed by Hoechst 33,342 staining showing nuclear condensation. UA also caused mitochondrial membrane depolarization, as indicated by JC-1 staining. Western blot analysis showed significant upregulation of P53 and the pro-apoptotic protein BAX (p < 0.01), and downregulation of the anti-apoptotic protein Bcl-2 (p < 0.01) following UA treatment. This study is the first to show that UA induces apoptosis in NPC cells by activating the P53 signaling pathway using network pharmacology and experimental validation.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"189"},"PeriodicalIF":2.8,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144021422","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":"Emerging nanostructure-based strategies for breast cancer therapy: innovations, challenges, and future directions.","authors":"Saqib Hussain Hadri, Atiya Riaz, Jaisha Abid, Rameeza Shaheen, Samreen Nadeem, Zainab Ghumman, Hammad Naeem","doi":"10.1007/s12032-025-02743-z","DOIUrl":"10.1007/s12032-025-02743-z","url":null,"abstract":"<p><p>Breast cancer, one of the leading causes of cancer-associated deaths, is responsible for the majority of cases of cancer in women globally. Traditional therapies used for the treatment of cancer have some challenges such as low cellular absorption, multidrug resistance, and limited bioavailability. Current innovations in nanotechnology, such as nanoliposomes, silver nanoparticles, gold nanoparticles, and carbon nanotubes, provide a promising approach to deal with these limitations. Nanostructures encapsulating anticancer agents such as doxorubicin, curcumin, paclitaxel, erlotinib, and docetaxel enhance the therapeutic efficacy of these agents and promote targeted drug delivery. Curcumin-loaded amorphous calcium carbonate nanoparticles encapsulating lipids and L-arginine exhibit higher cytotoxicity than free curcumin. Gold nanoparticles can also enhance treatment efficacy by specifically destroying tumor cells when used in photothermal therapy. This review focus on the abilities of nanoparticles to induce oxidative stress, prevent proliferation, and trigger apoptosis in cancer cells. Further research should focus on optimizing these nanoparticles to enhance the targeted drug delivery and address multi-drug resistance. Our review underscores recent developments in nanostructures, their therapeutic potential, and the challenges that need to be addressed for more effective breast cancer treatment.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 6","pages":"188"},"PeriodicalIF":2.8,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144032215","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}