Current cancer drug targets最新文献

{"title":"FDFT1 Suppresses Ovarian Tumorigenesis and Overcomes Cisplatin Resistance by Activating Ferroptosis Through the NRF2/GPX4/SLC7A11 Axis.","authors":"Yu Jiang, Pincheng Li, Ximu Xiao, Shuai Zhen, Jiaojiao Lu","doi":"10.2174/0115680096458617260514091154","DOIUrl":"https://doi.org/10.2174/0115680096458617260514091154","url":null,"abstract":"<p><strong>Introduction: </strong>Ovarian cancer's lethality stems from late-stage diagnosis and chemoresistance. Ferroptosis induction represents a promising strategy to overcome platinum resistance. Farnesyl diphosphate farnesyltransferase 1(FDFT1), a cholesterol metabolism enzyme with paradoxical roles in cancer, remains relatively underexplored in ovarian carcinogenesis and therapeutic resistance.</p><p><strong>Method: </strong>Multi-omics analyses of public datasets identified FDFT1's clinical relevance. Functional studies employed FDFT1-overexpressing ovarian cancer cells (SKOV3/ES-2) and cisplatin-resistant SKOV3/DDP models. Mechanistic evaluations included ferroptosis markers (Fe²⁺, MDA, GSH), NRF2/GPX4/SLC7A11 axis analysis, and xenograft experiments.</p><p><strong>Results: </strong>FDFT1 showed recurrent genomic loss and downregulation in ovarian tumors. Overexpression suppressed proliferation, migration, and invasion, while increasing apoptosis. FDFT1 activated ferroptosis via NRF2/GPX4/SLC7A11 axis suppression, elevating Fe²⁺, MDA, and ROS while depleting GSH. Cisplatin-resistant tumors exhibited FDFT1 downregulation, and overexpression of FDFT1 reversed drug resistance. Xenografts confirmed tumor growth suppression with ferroptosis activation.</p><p><strong>Discussion: </strong>Our findings establish FDFT1 as a tumor suppressor that induces ferroptosis via NRF2/GPX4/SLC7A11 inhibition in ovarian cancer. Restoring FDFT1 reverses cisplatin resistance, linking its downregulation to chemoresistance. This contrasts with its oncogenic roles in other cancers, highlighting context-dependent metabolic regulation. These findings position FDFT1 as a novel regulator of ferroptosis and a promising therapeutic target for overcoming chemoresistance in ovarian cancer.</p><p><strong>Conclusion: </strong>FDFT1 functions as a tumor suppressor by inducing iron-dependent lipid peroxidation through NRF2 pathway inhibition. Its restoration overcomes cisplatin resistance, positioning FDFT1 as both a promising biomarker and therapeutic target for chemoresistant ovarian cancer.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257709","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":"Downregulation of TIMP1 Promotes Ferroptosis and Suppresses Proliferation and Migration of Gastric Cancer Cells via Modulation of the PI3K/AKT Pathway.","authors":"Yan Kang, Yaoqi Li, Tianxiang Liu, Chenglou Zhu, Junfeng Ma","doi":"10.2174/0115680096437140260605102156","DOIUrl":"https://doi.org/10.2174/0115680096437140260605102156","url":null,"abstract":"<p><strong>Introduction: </strong>Tissue inhibitor of metalloproteinase 1 (TIMP1) is essential for the development and progression of various cancers and represents a valuable prognostic indicator.</p><p><strong>Methods: </strong>The present study utilized in vitro experimental models and comprehensive bio-informatics analyses to systematically investigate the biological function of TIMP1 in gastric cancer.</p><p><strong>Results: </strong>We found a positive correlation between TIMP1 expression and clinical stage in gastric cancer patients. Silencing of the TIMP1 gene markedly impaired the proliferative, invasive, and migratory capacities of gastric cancer cells. Furthermore, downregulation of TIMP1 could retard gastric cancer progression by suppressing the PI3K/AKT signaling pathway, thereby triggering lipid peroxidation and ferroptosis in gastric cancer cells.</p><p><strong>Discussion: </strong>This study reveals that TIMP1 serves as a key regulator of ferroptosis in gastric cancer cells. Specifically, downregulation of TIMP1 inhibits the PI3K/AKT signalling pathway, reduces the intracellular antioxidant defense capacity (e.g., GPX4 and SLC7A11 expression), and consequently induces ferroptosis, accompanied by the suppression of malignant tumour phenotypes.</p><p><strong>Conclusion: </strong>This suggests that TIMP1 could serve as a novel biomarker, offering new perspectives on the molecular mechanisms underlying gastric cancer and its treatment.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148223537","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":"CXCR4 Facilitates Osteosarcoma Progression through MMP9-Mediated Cell Migration and Matrix Degradation.","authors":"Hanyong Zhang, Mengchang Xu, Yan Jiang, Jia Luo, Qin Tan, Ziyu Huang, Wenchang Shi, Ruiche Shi, Binsheng He","doi":"10.2174/0115680096459805260518192517","DOIUrl":"https://doi.org/10.2174/0115680096459805260518192517","url":null,"abstract":"<p><strong>Purpose: </strong>Osteosarcoma is a is a severe bone cancer type with a poor prognosis and limited therapies for metastatic. CXCR4 and MMP9 are connected to tumor dissemination and invasiveness, but their functional interaction in osteosarcoma remains unclear. We sought to elucidate the function of CXCR4 in promoting osteosarcoma cell migration and extracellular matrix breakdown by targeting MMP9.</p><p><strong>Methods: </strong>Osteoblasts (hFOB1.19) and osteosarcoma cells (MG-63, U2OS, 143B) were applied to examine the expression and role of CXCR4 and MMP9. Cells were transfected with CXCR4 siRNA, MMP9 siRNA, or overexpression plasmids. Functional assays including wound healing, Transwell invasion, qRT-PCR, Western blot, ELISA, and immunofluorescence were conducted. Rescue experiments were performed to validate the CXCR4-MMP9 regulatory axis.</p><p><strong>Results: </strong>CXCR4 and MMP9 were significantly upregulated in osteosarcoma cells compared with normal osteoblasts, with 143B cells showing the highest expression levels. CXCR4 silencing inhibited, whereas overexpression enhanced, cell migration, invasion, and matrix degradation. CXCR4 positively regulated MMP9 at transcriptional and functional levels, as illustrated by qRT-PCR, Western blot, ELISA. Overexpression of MMP9 in rescue experiments was able to partially negate the effects of CXCR4 knockdown, while MMP9 silencing attenuated the pro-invasive effects of CXCR4 overexpression. Co-localization of CXCR4 and MMP9 was confirmed by immunofluorescence staining.</p><p><strong>Conclusion: </strong>CXCR4 promotes osteosarcoma cell invasiveness through upregulation of MMP9. The CXCR4-MMP9 axis may represent a potential therapeutic target to limit osteosarcoma progression and metastasis.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204306","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":"Screening of Demethylation-related Biomarkers and Exploration of Regulatory Mechanisms in Esophageal Cancer Patients Based on Machine Learning and Mendelian Randomization.","authors":"Yi Sheng, Jie Ma, Yang Li, Zihuan Yin, Xukun Gao, Ruixing Luo, Boxiang Sheng, Xueying Zhu, Renquan Zhang","doi":"10.2174/0115680096448097260417093740","DOIUrl":"https://doi.org/10.2174/0115680096448097260417093740","url":null,"abstract":"<p><strong>Introduction: </strong>The aggressive cancer known as Esophageal Squamous Cell Carcinoma (ESCC) has a dismal prognosis. Epigenetic changes such as demethylation have a significant impact on ESCC development and progression.</p><p><strong>Methods: </strong>WGCNA and differential expression analysis of GEO datasets identified tumorrelated demethylation genes. Random Survival Forest (RSF), univariate Cox regression, and LASSO-Cox models were employed to further screen prognostic genes and establish risk prediction models. Drug sensitivity and immune infiltration analyses were used to evaluate therapeutic implications. Mendelian Randomization (MR) assessed the genetic causality of key genes. Single-cell RNA sequencing elucidated cellular heterogeneity, intercellular communication, and differentiation trajectories in the tumor microenvironment. Finally, qPCR validated key gene expression in both ESCC tumor tissues and adjacent normal tissues.</p><p><strong>Results: </strong>Integrating co-expression with differential expression analyses enabled the identification of 150 demethylation genes associated with tumors. Six key prognostic genes (SERPINH1, PLAU, ANO1, RAB25, MAGEA4, and COL2A1) were selected to develop a risk prediction model, which showed improved accuracy after integrating clinical variables Age and Stage. Risk scores positively correlated with tumor stage and patient age, with higher scores predicting increased sensitivity to cisplatin, docetaxel, and vinorelbine. Immune infiltration analysis revealed reduced neutrophil levels associated with key gene expression. MR identified PLAU and RAB25 as causally linked to ESCC. Single-cell transcriptome and cell communication analyses highlighted squamous epithelial cells and altered LAMININ signaling in tumors. qPCR and expression analysis verified the expression of key genes.</p><p><strong>Discussion: </strong>This study identifies demethylation-driven prognostic genes as possible targets for treatment and biomarkers for precision management of ESCC.</p><p><strong>Conclusion: </strong>Six prognostic genes, particularly RAB25 and PLAU, influence ESCC progression and immune microenvironment remodeling.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204388","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":"Scorpion Venom-Derived Voltage-Gated Potassium Channel Blocker Peptides: A Cutting-Edge Therapeutic Frontier in Breast Cancer Research and Beyond.","authors":"Fatemeh Kazemi-Lomedasht, Mohammad Hosein Ghaffari, Mohammad Amir Esmaeili, Seyedeh Narges Fatemi, Zohre Eftekhari","doi":"10.2174/0115680096411088251126054847","DOIUrl":"https://doi.org/10.2174/0115680096411088251126054847","url":null,"abstract":"<p><p>Recent advancements in breast cancer research suggest that potassium channel blocker peptides from scorpion venom could serve as innovative therapies. Ion channels, particularly Voltage-Gated Potassium Channels (VGKCs), are therapeutic targets. They are regularly overexpressed in breast cancer tissues and play critical roles in proliferation, tumor progression, angiogenesis, and apoptosis. VGKCs also affect voltage-sensitive Ca2+ channels by regulating membrane potential and Ca2+ influx, which is vital for processes associated with cancer cell behavior. Scorpion venoms, rich in peptide toxins, specifically target these potassium channels, with the α-KTx family being notable for their high binding affinity and significant influence on therapeutic outcomes. Understanding the mechanisms of these toxins is crucial, primarily because potassium channel dysfunction is associated with various conditions, including cancer. Traditional treatments often prove ineffective for TNBC due to the deficiency of specific receptor expression, highlighting the need for alternative approaches like scorpion venom peptides. The distinctive properties of ion channels, especially the modifiable Kv10.1 and Kv1.3 channels, make them therapeutic targets, as their blockers exhibit anti-proliferative effects. VGKCs play a significant role in cell proliferation and apoptosis, and their modulation by scorpion venom peptides can impact the survival and growth of cancer cells. Additionally, the peptide's interaction with ion channels can alter membrane potential and calcium influx, thereby altering cancer cell behavior. This research lays the groundwork for future studies examining the mechanisms and specificity of scorpion venom-derived peptides, paving the way for translating these findings into clinical advancements in breast cancer therapies.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204415","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":"Rare ALK-IR (Intergenic Region) Rearrangement in a Patient with Non-Small Cell Lung Cancer: A Case Report.","authors":"Qingtao Ni, Chi Pan, Guangzhi Sun, Jianping Song, Quan Chen, Peng Wang","doi":"10.2174/0115680096433153251111154000","DOIUrl":"https://doi.org/10.2174/0115680096433153251111154000","url":null,"abstract":"<p><strong>Introduction: </strong>Non-small cell lung cancer (NSCLC) accounts for most lung cancer cases, with anaplastic lymphoma kinase (ALK) rearrangement being a key driver in some instances. The identification of oncogenic drivers in lung cancer has transformed the therapeutic landscape of NSCLC management. Developing and using specific ALK inhibitors have markedly improved clinical outcomes in patients with ALK-positive tumors.</p><p><strong>Case description: </strong>A 42-year-old male presented with hoarseness and was diagnosed with lung adenocarcinoma through lymph node biopsy. A positron emission tomography-computed tomography (PET-CT) revealed a right upper lobe mass with extensive nodal metastases. Immunohistochemistry confirmed ALK positivity, and next-generation sequencing identified a novel ALK-IR (intergenic region) rearrangement (19.09% abundance), along with mutations in tumor protein 53 (TP53) and cyclin-dependent kinase inhibitor 2A (CDKN2A). To our knowledge, this is the first report of an ALK-IR rearrangement in NSCLC. The patient was treated with crizotinib (250 mg twice daily), achieving partial remission with symptom resolution and no adverse effects over 17 months.</p><p><strong>Conclusion: </strong>This first documented case demonstrates the therapeutic efficacy of crizotinib in ALK-IR rearranged NSCLC, emphasizing the importance of comprehensive molecular profiling in guiding precision oncology.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204355","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":"AAV-HOTAIR Delivery in Colorectal Cancer Cells: Preliminary Insights into Gene Silencing and Epigenetic Influences.","authors":"Mohammed Y I Al-Hamadani, Firas H Khathayer, Mohammed N Al-Khafaf, Haitham A Rajab, Wael M El-Sayed","doi":"10.2174/0115680096443654260330053221","DOIUrl":"https://doi.org/10.2174/0115680096443654260330053221","url":null,"abstract":"<p><strong>Introduction: </strong>Colorectal cancer (CRC) remains a common and aggressive malignancy worldwide, highlighting the need for novel strategies to study and modulate disease-relevant pathways. This study aims to evaluate the feasibility of Adeno-Associated Virus-mediated HOTAIR silencing (AAV-HOTAIR) in CRC cells, focusing on delivery efficiency, gene expression modulation, and the influence of epigenetic context.</p><p><strong>Methods: </strong>Caco-2 (CRC) and WI-38 (normal fibroblast) cell lines were used to assess AAV-HOTAIR penetration, cell viability, and expression of key oncogenes and tumor suppressors (KRAS, NF-κB, and p53). DNA methylation effects were explored using bisulfite-mediated CpG island analyses.</p><p><strong>Results: </strong>AAV-HOTAIR transduction was higher in Caco-2 cells (84%) than in WI-38 cells (16%), and was associated with a 21% reduction in CRC cell viability, while WI-38 cells remained largely unaffected. Gene expression analysis showed a 77% decrease in KRAS, an 83% decrease in NF-κB, and an 85% increase in p53 in Caco-2 cells. CpG demethylation conditions influenced these trends, suggesting that epigenetic background can modulate cellular responses to HOTAIR silencing. Consistently, cleaved caspase-3 activity increased in transfected Caco-2 cells, confirming induction of apoptosis, while remaining unchanged in WI-38 cells.</p><p><strong>Discussion: </strong>These findings provide preliminary evidence that AAV-mediated HOTAIR silencing is feasible and can selectively modulate oncogenic and tumor suppressor pathways in CRC cells. The observed effects were influenced by epigenetic context, underscoring the importance of accounting for DNA methylation in future studies. This work establishes a foundational framework for evaluating lncRNA-targeted delivery strategies in CRC.</p><p><strong>Conclusion: </strong>AAV-mediated HOTAIR silencing represents a promising approach for modulating CRC-associated molecular pathways. Further mechanistic and functional investigations, including apoptosis assays and expanded cell line panels, are warranted to validate and extend these findings.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197588","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 Drug Metabolism for Triple Negative Breast Cancer: A Systematic Review.","authors":"Sakshi Singh, Swaroop Kumar Pandey, Jagdip Singh Sohal","doi":"10.2174/0115680096429469251212053118","DOIUrl":"https://doi.org/10.2174/0115680096429469251212053118","url":null,"abstract":"<p><strong>Introduction: </strong>The global rise in breast cancer incidence and associated mortality remains a pressing public health concern. Despite advancements in diagnostic modalities and the availability of diverse therapeutic strategies, mortality rates continue to escalate, particularly in aggressive subtypes, such as triple-negative breast cancer (TNBC).</p><p><strong>Materials and methods: </strong>A thorough systematic review of literature relevant to the theme of this article was conducted using PubMed, Google Scholar, ScienceDirect, and other databases, applying a six-year filter. Figures related to breast cancer prevalence were obtained from the webpage of the Global Cancer Observatory.</p><p><strong>Results: </strong>Strategic modulation of metabolic circuits holds promise for reversing resistance phenotypes. Drug-metabolizing enzymes represent a compelling therapeutic target due to their diverse isoforms and broad substrate specificity in xenobiotic metabolism. Employing selective inducers or inhibitors of these enzymes may enhance drug bioavailability and potentiate complete pathological responses.</p><p><strong>Discussion: </strong>This systematic review examines targeted approaches to managing TNBC by modulating metabolic pathways and drug-metabolizing enzymes. These enzymes and pathways exhibit differential expression patterns across cancer subtypes, often driving resistance mechanisms. Furthermore, emerging challenges and evolving trends in TNBC therapy and drug development are addressed, emphasizing the need for precision-targeted interventions to tackle the unique metabolic landscape of resistant tumors.</p><p><strong>Conclusion: </strong>Overcoming drug resistance is critical for enhancing chemotherapeutic outcomes and minimizing systemic toxicity associated with high-dose regimens. Targeting metabolic pathways involved in breast cancer progression, as well as drug-metabolizing enzymes, can be a vital strategy to circumvent drug resistance in both hormone receptor-positive and hormone receptor-negative breast cancers.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197676","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":"Leveraging a Disulfidptosis-related LncRNA Prognostic Signature to Indicate Immune Features and Drug Sensitivity of Gastric Cancer Based on Machine Learning.","authors":"Xinyu Pan, Mei Yang, Lilan Fan, Guoqingyuan Li, Ranran Zhang, Jing Liu","doi":"10.2174/0115680096427239260209013858","DOIUrl":"https://doi.org/10.2174/0115680096427239260209013858","url":null,"abstract":"<p><strong>Introduction: </strong>Disulfidptosis is a newly identified, programmed cell death that could influence the progression, immune microenvironment, and therapeutic response of stomach adenocarcinoma (STAD). This mechanism is potentially regulated by long non-coding RNAs (lncRNAs).</p><p><strong>Materials and methods: </strong>We analyzed TCGA datasets to identify 187 disulfidptosis-related lncRNAs (DRlncRNAs). Prognostic candidates were screened using univariate Cox, LASSO, and multivariate Cox analyses. Molecular subtypes were stratified via consensus clustering. Additionally, we construct a prognostic model based on key DRlncRNAs and evaluate its clinical relevance in terms of immune infiltration, functional pathways, drug responsiveness, and tumor mutation burden (TMB). Finally, expression validation of these DRlncRNAs was performed in STAD cell lines using qRT-PCR.</p><p><strong>Results: </strong>We established a three-DRlncRNA prognostic model demonstrating robust predictive performance with high AUC values. Patients in the low-risk subgroup exhibited favorable survival outcomes and greater sensitivity to immunotherapy. Conversely, the high-risk subgroup showed reduced survival, increased tumor malignancy, and poorer response to immunotherapy. qRT-PCR validation revealed significant expression differences of these three DRlncRNAs between gastric cancer cell lines and normal gastric epithelial cell lines.</p><p><strong>Discussion: </strong>DRlncRNAs were identified as potential biomarkers for prognostic and immune profiling in STAD. The identified signature may reflect biological activities associated with disulfidptosis and suggest potential therapeutic targets. Further mechanistic and translational studies are needed to determine whether these DRlncRNAs directly regulate disulfidptosis and to support clinical applications.</p><p><strong>Conclusion: </strong>This DRlncRNA-based prognostic model demonstrates strong predictive power for survival outcomes in STAD, offering guidance for personalized treatment strategies.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148143050","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":"Precision Strategies for Normal Tissue Radiotoxicity: Biomarkers, AI, and Nanomedicine in Clinical Practice.","authors":"Sonu Singh Ahirwar, Jagat Rakesh Kanwar, Ashwin Kotnis","doi":"10.2174/0115680096394588250910212641","DOIUrl":"https://doi.org/10.2174/0115680096394588250910212641","url":null,"abstract":"<p><p>Radiation therapy is a globally used treatment modality for head and neck cancer (HNC). However, its effectiveness is often constrained by radiation toxicity, which adversely affects patient outcomes and quality of life. DNA damage repair genes play a critical role as predictors of radiation-induced toxicity, paving the way for personalized treatment approaches. Emerging technologies, such as nanotechnology and artificial intelligence (AI), provide innovative strategies to mitigate these adverse effects and enhance therapeutic precision. This narrative review analyzes the current literature from PubMed, Scopus, Web of Science, and Google Scholar to investigate the role of genetic biomarkers, nanotechnology, and AI in managing radiation-induced normal tissue toxicity in HNC patients. Genetic biomarkers serve as predictive tools for identifying normal tissue side effects of radiation therapy in HNC patients. Nanoparticles enhance tumor targeting, while AI personalizes radiation therapy, improving precision and minimizing side effects. Integrating genetic biomarkers, nanotechnology, and AI into radiation therapy holds transformative potential to reduce normal tissue toxicity and improve outcomes for HNC. Overcoming existing challenges is essential for the successful clinical implementation of these innovations.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147980828","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}