Medical Oncology最新文献

{"title":"Tumor microenvironment and immunotherapy: from bench to bedside.","authors":"Avipsa Sinha, Debasmita Ghosh, Dipanjan Karati","doi":"10.1007/s12032-025-02818-x","DOIUrl":"10.1007/s12032-025-02818-x","url":null,"abstract":"<p><p>The tumor microenvironment (TME) is a multifaceted and ever-changing assemblage of cells and extracellular constituents. These components are closely linked to the onset and progression of malignancies, as well as their treatment. The TME is characterized by aberrant vasculature, altered extracellular matrix, immune cells, secreted factors, and cancer-associated fibroblasts and macrophages. The importance of the tumor microenvironment (TME) in understanding the course of cancer and resistance to treatment has been highlighted. The TME can suppress immune responses and promote tumor survival by inducing immunosuppressive mechanisms, such as regulatory T cells, myeloid-derived suppressor cells (MDSCs), and checkpoint molecule expression (e.g., PD-L1). Recent research has focused on understanding the interactions between immune cells within the TME to develop strategies that can remodel this environment and increase the effectiveness of immunotherapy. However, the efficacy of immunotherapeutic strategies is frequently hindered by the immunosuppressive nature of the TME. This abstract explores how these dynamics have led to the development of novel immunotherapeutic strategies aimed at reprogramming the TME to enhance antitumor immune responses. Novel approaches targeting TME therapy, such as immune checkpoint blockade (ICB), metabolic inhibitors, and key enzymes of immune metabolism, have been used to treat of cancer immunotherapy. Additionally, new and promising treatments including CAR-T cell therapy, oncolytic viruses, and cytokine-mediated TME modulation have shown promising results. This review provides a general overview of the TME, its components, its impact on immunotherapy outcomes, and emerging approaches to enhance therapeutic efficacy by remodeling the TME.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 7","pages":"244"},"PeriodicalIF":2.8,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248613","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 approach: inclusion complex-capped gold nanoparticles for paclitaxel delivery in triple-negative breast cancer.","authors":"Kamini Velhal, Parvinder Sah, Rajesh Raut, Ramesh Yamgar, Revanth Naidu, Palak Kalra, Sagar Barage, Jaya Lakkakula, Imran Uddin","doi":"10.1007/s12032-025-02805-2","DOIUrl":"10.1007/s12032-025-02805-2","url":null,"abstract":"<p><p>As possible delivery systems for anticancer medications and molecular imaging, polymer nanoparticles have tremendous potentials. This study aimed to develop a novel drug delivery system using PTX conjugated β-cyclodextrin inclusion complex-capped gold nanoparticles (PTX-β-CD-AuNPs) to manage triple-negative breast cancer (TNBC). Characterization techniques confirmed the successful synthesis of PTX-β-CD-AuNPs with mean size of around 43 nm. In vitro studies demonstrated enhanced cytotoxicity of PTX-β-CD-AuNPs compared to the individual components, as evidenced by MTT assay results. Furthermore, morphological analysis revealed significant alterations in cancer cell morphology, including cytoskeletal disruption and apoptosis induction. The clonogenic assay demonstrated the ability of PTX-β-CD-AuNPs to suppress colony formation, indicating potential targeting of cancer stem cells. Additionally, migration assays showed reduced cell migratory capacity, suggesting potential anti-metastatic effects. These findings illustrate the efficacy of PTX-β-CD-AuNPs as a promising nanocarrier for treating TNBC. To assess the therapeutic efficacy of PTX-β-CD-AuNPs and clarify the mechanisms behind it, additional study is essential.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 7","pages":"243"},"PeriodicalIF":2.8,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248608","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":"CEBPB regulates ERK1/2 activity through SOS1 and contributes to ovarian cancer progression.","authors":"Jiahong Tan, Daoqi Wang, Aiqing Tu, Qin Xu, Li Zhuan, Xiaodie Wu, Lin Zhao, Wei Dong, Jie Zhang, Yun Feng","doi":"10.1007/s12032-025-02794-2","DOIUrl":"10.1007/s12032-025-02794-2","url":null,"abstract":"<p><p>Ovarian cancer (OC) is among the most prevalent malignant tumors affecting the female reproductive system. Notably, CEBPB has emerged as a highly promising biomarker, attracting substantial attention for its role in mediating chemotherapy resistance to PARP inhibitors (PARPi). However, the precise mechanism of action of CEBPB in OC remains poorly understood. CCK-8 assays, colony formation assays, transwell assays, and wound healing assays were employed to assess malignant behaviors of OC cells. Flow cytometry was utilized to analyze cell apoptosis and cell cycle progression. qRT-PCR and Western blot analyses were performed to quantify the levels of SOS1 and phosphorylated ERK1/2 (p-ERK1/2). Overexpression of CEBPB enhanced the proliferation, colony formation ability, invasion, migration, and cell cycle progression of SKOV3 and A2780 OC cells, while simultaneously inhibiting their apoptosis. Conversely, knockdown of CEBPB produced opposite effects (p < 0.01). Results from the MAPK Signaling Pathway PCR Array and Western blot analyses indicated that CEBPB increases the expression of SOS1 (p < 0.01). Additionally, dual-luciferase reporter assays demonstrated that CEBPB binds to the promoter sequence of the target gene SOS1. CEBPB knockdown significantly inhibited the malignant behavior of OC cells and reduced the levels of p-ERK1/2, whereas overexpression of SOS1 partially reversed this effect (p < 0.01). In xenograft models, CEBPB activates ERK1/2 via SOS1 upregulation, which subsequently promotes tumor growth and suppresses apoptosis (p < 0.01). CEBPB regulates ERK1/2 activity through SOS1 and contributes to OC progression.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 7","pages":"242"},"PeriodicalIF":2.8,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12145290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gilteritinib suppresses prostate cancer cell proliferation and migration and induces ER stress-mediated non-autophagic cytoplasmic vacuolization cell death.","authors":"Gaurav Jha, Bhawna Tomar, Sakshi Mishra, Divyansh Sharma, Radhika Kapoor, Sonam Kanchan, Sushma, Srikanta Kumar Rath","doi":"10.1007/s12032-025-02803-4","DOIUrl":"10.1007/s12032-025-02803-4","url":null,"abstract":"<p><p>Prostate cancer (PCa) is a leading malignancy among men and lacks effective treatment, particularly for metastatic stages. Metastasis contributes significantly to cancer morbidity and mortality. Gilteritinib showed anticancer activity against lung and colorectal cancer but has not been thoroughly investigated for its potential in PCa therapy. This study evaluated the anticancer effects of gilteritinib on PCa cell lines (PC3 and DU145) by assessing cytotoxicity, cell proliferation, colony formation, and migration. Mechanistic studies were conducted to determine its impact on the cell cycle, epithelial-to-mesenchymal transition (EMT), and Wnt/β-catenin signaling. Additionally, the mode of cell death was explored, focusing on endoplasmic reticulum (ER) stress and protein ubiquitination. Gilteritinib exhibited dose-dependent cytotoxicity and inhibited PCa cell proliferation, colony formation, and migration. It induced G1 phase cell cycle arrest by downregulating CDK2, CDK4, and cyclin E1. EMT modulation was observed through the suppression of vimentin, N-cadherin, and Twist, along with increased E-cadherin expression. This EMT inhibition correlated with the downregulation of Wnt/β-catenin signaling components. Notably, gilteritinib triggered a non-apoptotic, non-autophagic cell death characterized by cytoplasmic vacuolation, ER stress, and protein ubiquitination, requiring new protein synthesis. This effect was mediated through the activation of the unfolded protein response (UPR) via the PERK pathway. Gilteritinib demonstrates significant anticancer potential in PCa by inducing cell cycle arrest, inhibiting EMT, suppressing Wnt/β-catenin signaling, and triggering a unique mode of cell death via ER stress. These findings highlight gilteritinib as a promising therapeutic candidate for PCa treatment.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 7","pages":"241"},"PeriodicalIF":2.8,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248611","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":"Investigating the impact of berberine on autophagy-mediated drug resistance in chronic lymphocytic leukemia tumor cells.","authors":"Ghazaleh Alizad, Maral Hemati, Bahador Bagheri, Parviz Kokhaei, Ali Memarian","doi":"10.1007/s12032-025-02779-1","DOIUrl":"10.1007/s12032-025-02779-1","url":null,"abstract":"<p><p>The persistence of drug resistance and relapses post-remission in B-chronic lymphocytic leukemia (B-CLL) underscores the exploration of novel therapeutic interventions. Given the pivotal role of autophagy in cancer cell resistance to apoptosis, this study aims to investigate the therapeutic potential of Berberine in modulating autophagy function associated with drug resistance in B-CLL. Peripheral blood mononuclear cells (PBMCs) from 10 CLL patients and 5 healthy individuals were treated with Berberine and Idelalisib (as a control). Flow cytometry analysis was employed to assess the protein expression levels of Beclin1, indicative of autophagy function, and high mobility group protein 1 (HMGB1), serving as an internal control for drug resistance. Furthermore, qRT-PCR was utilized to measure the expression levels of drug resistance markers including Beclin1, HMGB1, heat shock factor binding protein 1 (HSBP1), and receptor for advanced glycation end products (RAGE). Our findings revealed that Berberine exhibited a dual suppressive effect on Beclin1 and HMGB1 levels compared to the control drug. Moreover, Berberine downregulated the expression of the primary HMGB1 receptor, RAGE, in PBMCs from CLL patients. Notably, no significant alteration was observed in HSBP1 expression, a mediator of autophagy induction, upon Berberine treatment. These findings suggest that Berberine may target specific mechanisms associated with autophagy-mediated drug resistance, underscoring its therapeutic potential in B-CLL. Further clinical trials are warranted to validate the therapeutic efficacy of Berberine in B-CLL.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 7","pages":"240"},"PeriodicalIF":2.8,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234435","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":"Integration of immunotherapy and radiotherapy in a therapeutic algorithm for locally advanced squamous cell skin cancer.","authors":"Ioannis M Koukourakis, Antonios Karpouzis, Konstantinos Filippatos, Panagiotis Mamalis, Despina Kakagia, Alexandra Giatromanolaki, Vassilis Kouloulias, Anna Zygogianni, Michael I Koukourakis","doi":"10.1007/s12032-025-02785-3","DOIUrl":"10.1007/s12032-025-02785-3","url":null,"abstract":"<p><p>Locally advanced squamous cell skin cancer (LA-sqCSC) affects older patients who initially decline medical assistance and patients after multiple surgical interventions for recurrent tumors. Radical radiotherapy (RT) often becomes difficult to apply due to large surface areas, extensive ulceration, and tissue necrosis. Thirty patients with LA-sqCSC were treated according to a therapeutic algorithm involving upfront immunotherapy (IO) with cemiplimab (anti-PD-1 MoAb) and RT. Patients with progressive or stable disease (PgD, SD) or partial/minimal response (PR/MR) received local RT (6 daily fractions of 6 Gy) concurrently with cemiplimab. Complete responders (CR) after IO continued cemiplimab, till progression or development of immune-related adverse events (irAEs) for a maximum of 18 months. irAEs enforced interruption of cemiplimab in 6/30 (20.0%) patients. After the 6th cycle of IO, the CR rates were 50.0%. Nine patients with PR/MR to IO underwent RT. Six of them (66.7%) responded completely. The overall CR rates of patients treated with the proposed algorithm were 70.0%. The 2-year projected locoregional progression-free survival was 68.4% and the disease-specific overall survival was 85.2%. LA-sqCSC can be effectively treated with upfront cemiplimab IO followed by a short course of hypofractionated RT directed to the residual tumor.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 7","pages":"238"},"PeriodicalIF":2.8,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12137472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing the potential of nanoparticles for cancer detection and precision therapeutics.","authors":"Muhammad Naeem Kiani, Hamza Khaliq, Muhammad Abubakar, Merium Rafique, Fazliddin Jalilov, Ghulam Abbas Ashraf, Amel Ayari-Akkari, Ali Akremi","doi":"10.1007/s12032-025-02782-6","DOIUrl":"10.1007/s12032-025-02782-6","url":null,"abstract":"<p><p>Cancer poses a significant challenge with high death rate marked by heterogeneity, complexity, and resistance to available treatments, hence requiring creative approaches to improve early detection and precision medicines. Nanoparticles (NPs) exhibit distinctive physicochemical characteristics, including a high surface area-to-volume ratio, adjustable size and shape, and multifunctionality. This review paper critically explored the recent advancements in various NPs, such as graphene-based materials (to overcome cancer resistance and for diagnostic and therapeutics applications), metal organic frameworks (precised and targeted release of drug, e.g., glutathione-sensitive disulfide bonds for intracellular delivery), carbon dots, rhodamine 6G, polymer-based nanoformulation (CAP/ZnO NPs for lung cancer therapy), gold NPs (as radiosensitizing action), nanocarrier systems (including epigenetic control systems), aptamers, mesoporous polydopamine-based nanodrug, polymeric NPs, pH-responsive polymeric nanostructures (particularly in acidic tumor environment), multifunctional NPs, and carbon coated ferrite nanodots for targeted delivery to cancer cells. We, particularly, investigated their dual abilities in precise drug delivery of several payloads, like small molecules, proteins, and nucleic acids, in addition to their capabilities for real-time monitoring of therapeutic response in malignant cells. Moreover, this review underscores how the integration of Artificial Intelligence and machine learning algorithms with such NPs-based architectures is improving diagnostic precision and facilitating personalized cancer therapy approaches, navigating obstacles, including bioavailability and multidrug resistance. By evaluating critical recent breakthroughs about the role of nanotechnology in precision cancer therapy, this review paper highlights the pioneering capabilities of such intelligent nanomedicines in impacting cancer development, consequently advancing patient outcomes.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 7","pages":"239"},"PeriodicalIF":2.8,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225880","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":"Antitumor effect of BC12-3 on multiple myeloma via proteasome inhibition.","authors":"Huiying Li, Geng Jia, Naixin Zhang, Rui Fan, Wenqing Jia, Meihua Jin, Shingo Dan, Wennan Zhao, Yuqi Jiang, Dexin Kong","doi":"10.1007/s12032-025-02804-3","DOIUrl":"10.1007/s12032-025-02804-3","url":null,"abstract":"<p><p>Multiple myeloma (MM) ranks second only to lymphoma among hematologic malignancies in terms of incidence. Current treatment methods primarily rely on proteasome inhibitors (PIs) targeting the ubiquitin proteasome system (UPS). However, existing PIs regimens encounter several limitations, including severe adverse effects, rapidly developing resistance during treatment, and restricted therapeutic efficacy. In light of this, our work aims to explore strategies to mitigate poor conditions. We employed a systematic structural optimization process to design and synthesize the new compound BC12-3, based on prevailing PIs. JFCR39 COMPARE analysis was used to assess cytotoxic activity against 39 characteristic cancer cell lines, and the IC₅₀ value of BC12-3 was measured using CCK-8 assay. Cell cycle distribution and apoptosis were analyzed by flow cytometry, while western blotting investigated the antitumor mechanism of BC12-3. In vivo efficacy and safety of BC12-3 and bortezomib (BTZ) were evaluated in the xenograft model. ADMET computational analyses estimated the biological safety of these two inhibitors. As a result, BC12-3 exhibited potent broad-spectrum antitumor activity in vitro particularly against MM cells; This effect was achieved by selectively inhibiting β5 subunit of proteasome activity. BC12-3 suppressed MM cell growth primarily via cell cycle arrest in G2/M phase and apoptosis induction, the related molecular pathways confirmed these phenomena. In vivo studies indicated that BC12-3 exhibits significant effect in inhibiting tumor growth, with its efficacy comparable to that of the standard therapeutic drug, BTZ. Additionally, this new compound showed an excellent safety profile. Consequently, BC12-3 holds promise as a novel therapeutic strategy for the treatment of MM.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 7","pages":"235"},"PeriodicalIF":2.8,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216281","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 Gastrointestinal Cancers with Cannabidiol: Mechanisms, Challenges, and Therapeutic Implications.","authors":"Mojtaba Esmaeli, Maryam Dehghanpour Dehabadi","doi":"10.1007/s12032-025-02790-6","DOIUrl":"10.1007/s12032-025-02790-6","url":null,"abstract":"<p><p>Cannabidiol (CBD), a non-psychoactive compound derived from cannabis, has gained significant attention for its potential therapeutic effects across various types of cancer. This manuscript presents a systematic review of the current evidence on the application of CBD in gastrointestinal (GI) malignancies, with a focus on gastric and colorectal cancers. The review aims to explore CBD's mechanisms of action, including its effects on apoptosis, cell cycle regulation, angiogenesis, inflammation, and its potential to enhance the efficacy of conventional therapies. Furthermore, it examines the challenges involved in translating preclinical findings into clinical settings, such as issues related to bioavailability and regulatory hurdles. The review also addresses future directions for the use of CBD in combination therapies and its potential to overcome resistance mechanisms in GI cancers. By analyzing the molecular pathways modulated by CBD, this manuscript seeks to offer a comprehensive understanding of its therapeutic potential, contributing to the future of GI cancer treatment.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 7","pages":"237"},"PeriodicalIF":2.8,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216283","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":"ADAM22 enhances lymphatic metastasis and epithelial-mesenchymal transition in head and neck squamous cell carcinoma cells through integrin signaling.","authors":"Kai Yang, Yanshi Li, Kai Song, Min Pan, Tao Lu, Mengna Wang, Zhaobo Cheng, Guohua Hu, Tongling Wen, Min Wang, Tao Chen","doi":"10.1007/s12032-025-02789-z","DOIUrl":"10.1007/s12032-025-02789-z","url":null,"abstract":"<p><p>Lymphatic metastasis (LM) remains a major contributor to mortality among patients with head and neck squamous cell carcinoma (HNSCC). Understanding the molecular mechanisms underlying LM and identifying novel therapeutic targets are critical priorities. This study investigated ADAM22, a protein implicated in cell adhesion, migration, and differentiation, for its role in HNSCC and its association with LM. Its expression levels were evaluated in HNSCC tissues with and without LM using quantitative real-time PCR (qRT-PCR), western blotting, and immunohistochemistry. The prognostic relevance of ADAM22 was analyzed through Kaplan-Meier survival curves and Cox proportional hazards models. Functional assays, including EdU incorporation, flow cytometry, wound healing, and Transwell migration assays, were performed in FADU and SCC15 cell lines alongside an in vivo footpad xenograft mouse model. ADAM22 was found to be significantly overexpressed in HNSCC cases with LM. In vitro, silencing of ADAM22 suppressed tumor cell proliferation, migration, and invasion and promoted apoptosis. Both in vitro and in vivo experiments demonstrated that ADAM22 enhances tumor growth and lymphatic spread by promoting epithelial-mesenchymal transition (EMT). Further analysis identified integrins as key mediators in ADAM22-driven EMT and metastasis. In summary, these findings indicate that ADAM22 promotes LM in HNSCC by regulating EMT through integrin signaling, highlighting its potential as a therapeutic target and providing new perspectives for diagnosing and treating HNSCC.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 7","pages":"236"},"PeriodicalIF":2.8,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12133988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}