Oncology Research最新文献

{"title":"Current Advances in Preclinical Patient-Derived Cultivation Models for Individualized Drug Response Prediction in Pancreatic Cancer.","authors":"Benjamin Heckelmann, Jannis Duhn, Rüdiger Braun","doi":"10.32604/or.2026.075028","DOIUrl":"https://doi.org/10.32604/or.2026.075028","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is currently the third leading cancer-related cause of death worldwide and is forecasted to become the second leading cause in the United States by 2030. Despite the development of multimodal treatment regimens, 5-year overall survival remained as low as 12%. Several efforts have been made to account for different aspects of heterogeneous tumor biology in PDAC, aiming to enable treatment stratification of defined subtypes. Besides targeting specific mutations, the definition of molecular (transcriptional) subtypes has gained substantial interest regarding response prediction and treatment stratification. Despite numerous advances in the field of genomic, transcriptomic, and proteomic characterization, the identified biomarkers do not yet facilitate predicting treatment response sufficiently in patients <i>in vivo</i>. Considering the growing evidence on the impact of the tumor microenvironment (TME) and intratumoral heterogeneity (ITH) on treatment resistance, there is an unmet clinical need for preclinical cultivation models that allow for predicting treatment response based on individual biological criteria. This review discusses the current advances in such <i>in vivo</i> (patient-derived xenografts) and <i>ex vivo</i> (organoids, organotypic slice cultures, cancer-on-chip) models for treatment response prediction and stratification in PDAC, and their potential implications in clinical translation.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 5","pages":"1"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818182","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":"Integrative Machine Learning and Experimental Validation Identify MYBL2 as a Prognostic Biomarker and Therapeutic Target in Hepatocellular Carcinoma.","authors":"Ya-Ling Yang, Ying-Hsien Huang, Hung-Yu Lin","doi":"10.32604/or.2026.075284","DOIUrl":"https://doi.org/10.32604/or.2026.075284","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) presents with poor treatment outcomes, creating an urgent need for novel biomarkers to improve diagnosis, prognosis, and precision medicine. While the MYB family of oncogenes is implicated in cancer, the role and regulatory mechanisms of its member, particularly MYB proto-oncogene like 2 (MYBL2), remain underexplored in HCC. Therefore, this study aimed to systematically validate the clinical significance of MYBL2, elucidate its functional role in tumor progression and drug sensitivity, and identify its upstream regulatory mechanisms using an integrative machine learning and experimental framework.</p><p><strong>Methods: </strong>We applied an integrative pipeline combining LASSO-based feature selection on TCGA and GEO cohorts, single-cell transcriptomics, pharmacogenomic surveys, and CRISPR dependency screens. These computational approaches were complemented by <i>in vitro</i> HepG2 assays, luciferase reporter tests, iTRAQ proteomics, and an <i>in vivo</i> western diet/CCl₄ (WD/CCl₄) HCC model using miR-29a transgenic mice to investigate a putative regulatory axis.</p><p><strong>Results: </strong>MYBL2 robustly discriminated tumor from normal liver (AUC = 0.968), and high expression was associated with adverse features, including higher grade, microvascular invasion, HBV positivity, nonresponse to TACE, and worse survival. A nomogram combining MYBL2 with AJCC stage improved 1-, 3-, and 5-year AUCs versus stage alone. MYBL2 correlated with proliferative biomarkers (AFP, MKI67, PCNA, BIRC5) and CRISPR knockout inhibited growth in most HCC lines. High MYBL2 expression was associated with greater sensitivity to sorafenib in pharmacogenomic screens and was linked to an immunosuppressive microenvironment and higher MSI. Mechanistically, miR-29a was shown to suppress MYBL2 translation by directly binding to its 3^'-UTR; this was validated <i>in vivo</i>, where miR-29a transgenic mice were protected from WD/CCl₄-induced HCC, demonstrating reduced tumor burden, MYBL2 expression, and fibrosis. iTRAQ proteomics further confirmed MYBL2 as a top miR-29a-regulated protein.</p><p><strong>Conclusions: </strong>MYBL2 is a potent diagnostic and prognostic biomarker in HCC that also predicts sorafenib sensitivity. Our findings establish a clear regulatory link where MYBL2 is a direct and functionally important target of the tumor-suppressive miR-29a. This positions MYBL2 as a tractable target for miR-29a-based therapeutic strategies, warranting clinical validation for patient stratification and treatment development in HCC.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 5","pages":"26"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818439","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":"Targeting Oncogenic lncRNA KRT7-AS to Induce Ferroptosis Suppresses Ovarian Cancer Progression.","authors":"Yan Zhu, Bin Guan, Wencai Guan, Jihong Zhang, Shiyu Wang, Jimin Shi, Wei Fan, Qi Lu, Lingyun Zhang, Guoxiong Xu","doi":"10.32604/or.2026.075241","DOIUrl":"https://doi.org/10.32604/or.2026.075241","url":null,"abstract":"<p><strong>Background: </strong>Ovarian cancer poses the greatest threat to survival among gynecologic cancers in women. Long non-coding RNAs (lncRNAs) have emerged as critical regulators in oncogenesis. The current study aimed to elucidate the function and regulatory mechanism of lncRNA KRT7-AS in ovarian cancer.</p><p><strong>Methods: </strong>The clinical significance of KRT7-AS was evaluated through bioinformatics analysis of data from public repositories. KRT7-AS expression was examined by RT-qPCR and fluorescence <i>in situ</i> hybridization. The function analyses were conducted using assays for cell proliferation, migration, invasion, wound healing, and colony formation. Assessment of cell cycle and apoptosis was performed using flow cytometry. Mitochondrial membrane potential (MMP), reactive oxygen species (ROS), lipid peroxidation, and ferrous iron (Fe²⁺) levels were measured with specific kits. Tumor growth was assessed using a xenograft mouse model.</p><p><strong>Results: </strong>Patients exhibiting high KRT7-AS expression had a significantly lower survival rate. Functional assays demonstrated that KRT7-AS overexpression enhanced tumorigenic behaviors, including cell proliferation, invasion, and metastasis, whereas its knockdown suppressed these malignant phenotypes. KRT7-AS depletion induced ferroptosis, as indicated by increased MMP and ROS levels, and the accumulation of lipid peroxidation and Fe²⁺. In rescue experiments, the ferroptosis inhibitor ferrostatin-1 reversed the reduction in cell viability caused by KRT7-AS knockdown. Finally, <i>in vivo</i> studies showed that KRT7-AS knockdown inhibited tumor growth and modulated the expression of ferroptosis-related proteins by elevating ACSL4 and reducing GPX4.</p><p><strong>Conclusions: </strong>These findings suggest that KRT7-AS has potential as a diagnostic biomarker for ovarian cancer. Targeting KRT7-AS to induce ferroptosis may represent a promising therapeutic strategy for suppressing ovarian cancer progression.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 5","pages":"29"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126565/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818644","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":"A Novel Partial EMT-Associated Transcriptomic Signature for Prognostic Stratification in Ovarian Cancer.","authors":"Chia-Chia Chao, Cheng-Yao Lin, Po-Chun Chen, Wen-Tsung Huang, Teng-Song Weng, Sheng-Yen Hsiao","doi":"10.32604/or.2026.074383","DOIUrl":"https://doi.org/10.32604/or.2026.074383","url":null,"abstract":"<p><strong>Background: </strong>Partial epithelial-mesenchymal transition (p-EMT) is a dynamic cellular state associated with metastasis and adverse outcomes in multiple cancers, but its prognostic significance in ovarian cancer remains unclear. This study aimed to develop and validate an ovarian cancer-specific transcriptomic signature based on p-EMT-related genes, and to determine whether this signature can improve prognostic stratification and overall survival prediction across independent cohorts.</p><p><strong>Methods: </strong>A pan-cancer p-EMT gene set was curated from ten published studies. Using transcriptomic and clinical data from TCGA-OV (n = 488), a six-gene p-EMT signature was developed via LASSO regression to generate a patient-specific risk score. The score was integrated with clinical variables to construct a prognostic nomogram and validated in the external GEO cohort GSE140082 (n = 380) and GSE165808 (n = 51).</p><p><strong>Results: </strong>A six-gene p-EMT transcriptomic signature (ADAM9, ANXA8L1, FSTL3, RABAC1, TPM4, and TWIST1) was significantly associated with overall survival (OS) and stratified patients into high- and low-risk groups (adjusted HR = 1.74, <i>p</i> < 0.001). Incorporation with age and FIGO stage in a nomogram improved predictive performance, with AUCs of 0.727, 0.700, and 0.656 at 1-, 3-, and 5-year OS, respectively. External validation in GSE140082 and GSE165808 confirmed model robustness, yielding 3-year AUCs of 0.630 and 0.826, respectively, demonstrating preserved prognostic value across independent cohorts and disease stages.</p><p><strong>Conclusions: </strong>This six-gene p-EMT transcriptomic signature demonstrates prognostic value in ovarian cancer and offers potential for individualized risk stratification and clinical decisionsupport.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 5","pages":"27"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818605","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":"Targeting SRC/STAT3 Signaling Impairs Cancer Stem Cell Activity by Downregulation of Hexokinase-2 in Radioresistant Triple-Negative Breast Cancer Cells.","authors":"Yu-Hao Huang, Yu-Ci Tu, Peng-Ju Chien, An-Jie Lee, Chia-Liang Lin, Shao-Ti Li, Yueh-Chun Lee, Wen-Wei Chang","doi":"10.32604/or.2026.075190","DOIUrl":"https://doi.org/10.32604/or.2026.075190","url":null,"abstract":"<p><strong>Background: </strong>Triple-negative breast cancer (TNBC) is an aggressive subtype with poor prognosis and resistance to conventional therapies, including radiotherapy. Cancer stem cells (CSCs) drive tumor initiation, metastasis, and therapy resistance in TNBC. Identifying pathways sustaining CSCs in radioresistant TNBC is key for targeted therapies. This study examines SRC proto-oncogene (SRC) and the signal transducer and activator of transcription 3 (STAT3) activation in radioresistance and CSC maintenance.</p><p><strong>Methods: </strong>A radioresistant MDA-MB-231 TNBC cell line (231RR) was developed and compared to the parental line for CSC activity and self-renewal. Western blotting assessed molecular changes; functional assays followed SRC and STAT3 inhibitor treatment. SRCY^530F overexpression and hexokinase-2 (HK2) knockdown evaluated roles in CSC activity and signaling. Pathways were analyzed via metabolic assays, The Cancer Genome Atlas (TCGA) breast cancer datasets, and Harmonizome gene sets.</p><p><strong>Results: </strong>231RR cells exhibited enhanced CSC traits and upregulated SRC/STAT3 signaling, with heightened sensitivity to SRC/STAT3 inhibitors. Forced expression of SRCY530F in parental cells boosted STAT3 activation and CSC activity. SRC/STAT3 inhibition reduced HK2 without impairing glycolysis. HK2 knockdown decreased MYC proto-oncogene (c-MYC) and octamer-binding transcription factor-4 (OCT4). Finally, the suppression of epidermal growth factor receptor (EGFR) activation by gefitinib resulted in the inhibition of the SRC/STAT3/HK2 axis. TCGA data linked SRC to glycolytic signatures in breast cancer.</p><p><strong>Conclusions: </strong>The EGFR/SRC/STAT3/HK2 axis drives radioresistance and CSC maintenance in TNBC via HK2 upregulation. HK2 promotes stemness mainly through non-metabolic means, not broad metabolic shifts. Targeting this pathway could overcome radioresistance and enhance TNBC outcomes.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 5","pages":"25"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818625","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":"Extrachromosomal DNA in Solid Tumors-Landscape, Immune Effects, and Resistance to Targeted Therapy.","authors":"Omar Badran, Siraj Attarya","doi":"10.32604/or.2026.075916","DOIUrl":"https://doi.org/10.32604/or.2026.075916","url":null,"abstract":"<p><p>Extrachromosomal DNA (ecDNA) constitutes a principal factor in the amplification of oncogenes and the progression of tumors in solid malignancies. This review synthesizes emerging mechanistic, genomic, and immunologic evidence across multiple tumor types, including glioblastoma, lung, breast, gastrointestinal, hepatobiliary, urothelial, prostate, gynecologic, pediatric, and head-and-neck cancers, with the goal of clarifying the role of ecDNA in immune escape and therapy resistance and outlining its translational implications for precision oncology. ecDNA comprises substantial acentromeric circular elements that serve as transcriptional hubs, modulate enhancer-promoter interactions, and undergo dynamic copy-number cycling, thereby fostering intratumoral heterogeneity and resistance to therapy. Recurrent oncogenic cargos, including epidermal growth factor receptor (EGFR), v-myc avian myelocytomatosis viral oncogene homolog (MYC), erb-b2 receptor tyrosine kinase 2, also known as human epidermal growth factor receptor 2 (ERBB2/HER2), and cyclin D1 (CCND1), are frequently located in ecDNA. They can interconvert with intrachromosomal homogeneously staining regions (HSRs) under treatment pressure. Emerging evidence links ecDNA to an immune-cold phenotype, characterized by downregulation of antigen presentation and decreased responsiveness to immune checkpoint inhibitors. We further emphasize diagnostic and translational methodologies that incorporate ecDNA detection through liquid biopsy and the spatial mapping of tumor topology. Finally, we propose a comprehensive clinical implementation framework that integrates ecDNA profiling, longitudinal monitoring, and immune microenvironment assessment to guide precision therapy. Gaining a deeper understanding of ecDNA biology has the potential to ultimately transform it from merely a prognostic biomarker into a targetable element within cancer therapy.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 5","pages":"8"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818355","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":"Glutathione Peroxidases 1 and 3 Immunoscores in Clear Cell Renal Cell Carcinoma: New Insights from a Case-Series Study.","authors":"Dimitra P Vageli, Panagiotis G Doukas, Nikolaos Papageorgiou, Chrysanthi A Markou, Konstantina Zacharouli, Maria Ioannou","doi":"10.32604/or.2026.077195","DOIUrl":"https://doi.org/10.32604/or.2026.077195","url":null,"abstract":"<p><strong>Background: </strong>Renal cell carcinoma (RCC) is the most common type of kidney cancer in adults, with a poor prognosis in advanced stages. Although histological tumor grading is an established prognostic parameter, it often fails to capture the biological heterogeneity of RCC. Therefore, identifying novel biomarkers could enhance early diagnosis and improve predictive accuracy. Here, we aimed to test whether immunophenotypes of specific glutathione peroxidase (GPX) family members may have prognostic value in RCC.</p><p><strong>Methods: </strong>We investigated the relationship between GPX1 and GPX3 immunophenotypes and clinicopathological parameters in 32 surgical specimens of clear cell RCC (ccRCC) with nucleolar grade 1-4 (WHO/ISUP grading). We evaluated the GPX1 and GPX3 immunophenotypes and assigned a histological immunoscore for each marker. For analysis, we used Spearman and point-biserial correlation methods.</p><p><strong>Results: </strong>Our findings indicated a significant positive correlation between GPX1 immunoscore and high nucleolar grade (<i>r</i> = 0.80, <i>p</i> < 0.0001). In contrast, we observed a significant negative correlation between GPX3 immunoscore and high nucleolar grade (<i>r</i> = -0.77, <i>p</i> < 0.0001). We did not find statistically significant correlations between GPX1 expression and age, sex, tumor localization, or tumor size (<i>p</i> > 0.05), nor with capsular infiltration and invasion of the renal pelvis (<i>p</i> > 0.05). However, we did find statistically significant positive correlations between GPX1 expression and invasion of the renal vein (<i>p</i> = 0.038), perirenal fat (<i>p</i> = 0.043), and peripyelic fat (<i>p</i> = 0.015).</p><p><strong>Conclusion: </strong>Our data demonstrate that GPX1 and GPX3 immunophenotypes could have a prognostic role for ccRCC, particularly in relation to nucleolar grade. This study has limitations because of the small sample size; however, it underscores the necessity for further research in larger, prospective studies. These studies should more thoroughly examine the associations between GPX1 and GPX3 and clinicopathological parameters, and validate them as potential novel prognostic biomarkers.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 5","pages":"16"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818399","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":"Machine Learning (ML) and Molecular Dynamics-Driven Optimization of VEGFR2 Ligands against Hepatocellular Carcinoma.","authors":"Farzana Yasmeen, Abdul Manan, Wook Kim, Sangdun Choi","doi":"10.32604/or.2026.076072","DOIUrl":"https://doi.org/10.32604/or.2026.076072","url":null,"abstract":"<p><strong>Objectives: </strong>Vascular endothelial growth factor receptor 2 (VEGFR2) is a critical therapeutic target in hepatocellular carcinoma (HCC) due to its role in angiogenesis and tumor progression. While several inhibitors are currently used, clinical utility is often limited by resistance and adverse effects, necessitating the discovery of novel therapeutic agents. The aim of this study was to identify and characterize novel, highly effective VEGFR2 inhibitors using an integrated computational pipeline to advance the development of new HCC treatments.</p><p><strong>Methods: </strong>A comprehensive dataset from the ChEMBL database was curated and standardized for Quantitative Structure-Activity Relationship (QSAR) modeling. A binary classification framework was employed, where a Light Gradient Boosting Machine (LGBM) model demonstrated superior predictive performance. Two lead compounds and a reference were selected for in-depth molecular modeling. Their binding poses were predicted via molecular docking and subsequently subjected to 200 ns Molecular Dynamics (MD) simulations to assess stability and conformational dynamics. Thermodynamic binding affinities were calculated using the Molecular Mechanics Poisson-Boltzmann Surface Area (MMPBSA) method.</p><p><strong>Results: </strong>The LGBM model achieved high accuracy and a robust Matthews Correlation Coefficient (MCC) on an independent test set. MD analysis, including Root Mean Square Deviation (RMSD) and Radius of Gyration (Rg), confirmed stable binding throughout the 200 ns trajectory. MMPBSA calculations validated the binding affinities, identifying van der Waals and electrostatic interactions as the primary driving forces for complex stability.</p><p><strong>Conclusion: </strong>This study successfully bridges machine learning with advanced molecular simulations, offering a validated workflow for the rational design and optimization of novel small-molecule VEGFR2 inhibitors.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 5","pages":"24"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818484","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":"Retraction: miR-325-3p Promotes the Proliferation, Invasion, and EMT of Breast Cancer Cells by Directly Targeting S100A2.","authors":"","doi":"10.32604/or.2026.081623","DOIUrl":"https://doi.org/10.32604/or.2026.081623","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504020X16100888208039.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 5","pages":"39"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818515","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":"Retraction: MicroRNA-510 Plays Oncogenic Roles in Non-Small Cell Lung Cancer by Directly Targeting SRC Kinase Signaling Inhibitor 1.","authors":"","doi":"10.32604/or.2026.081621","DOIUrl":"https://doi.org/10.32604/or.2026.081621","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504018X15451308507747.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 5","pages":"38"},"PeriodicalIF":4.1,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126370/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147818519","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}