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  • Open Access

    ARTICLE

    PRDM1 Drives a TIM3+ Macrophage Immunosuppressive Niche via LGALS9 Signaling in Prostate Cancer Progression

    Yangyang Zhang1,2,3,#, Ilyar Mamtili4,#, Yonghao Chen5, Guangjie Ji1,2,3,*, Chaozhao Liang1,2,3,*

    Oncology Research, Vol.34, No.7, 2026, DOI:10.32604/or.2026.079316 - 16 June 2026

    Abstract Background: Prostate cancer (PCa) responds poorly to immunotherapy. We investigated the myeloid checkpoint TIM3 (HAVCR2) to define its lineage localization and regulatory logic in the PCa microenvironment. Methods: We integrated stage-resolved public single-cell RNA-seq datasets spanning primary PCa, metastatic hormone-sensitive PCa, and castration-resistant PCa. Myeloid compartments were analyzed via differential expression, regulon inference, and ligand–receptor modeling. Clinical relevance was evaluated in the Cancer Genome Atlas prostate adenocarcinoma (TCGA-PRAD) cohort and independent cohorts using a myeloid TIM3 signature. Mechanistic validation was achieved through PR domain zinc finger protein 1 (PRDM1) chromatin immunoprecipitation followed by Chromatin Immunoprecipitation (ChIP)–qPCR… More >

  • Open Access

    ARTICLE

    EBF1 Deficiency Drives Prostate Cancer Progression by Interfering with the Transcriptional Regulation of ITPR1

    Yuan Guo1,#, Hui Wang2,#, Xiaoyu Zhao3, Xiao Feng3, Xingjian Cai4, Wei Li3,*, Xiaohui Luo4,*

    Oncology Research, Vol.34, No.7, 2026, DOI:10.32604/or.2026.078850 - 16 June 2026

    Abstract Backgrounds: Early B-cell factor 1 (EBF1), originally identified as a critical transcription factor modulating the development and differentiation of B lymphocytes, has recently attracted significant interest owing to its diverse functional characteristics and regulatory mechanisms in solid tumors. Although current evidence suggests a potential connection between EBF1 and oncogenic developments, its exact role in the progression of prostate cancer (PCa) is unclear. This study sought to investigate its biological roles and regulatory mechanisms in human PCa. Methods: Bioinformatic analyses were performed utilizing Tumor Immune Estimation Resource (TIMER) 2.0, Gene Expression Profiling Interactive Analysis (GEPIA), and Gene… More >

  • Open Access

    REVIEW

    Clinical Application Progress of Artificial Intelligence in Pancreatic Cancer: From Diagnosis to Immunotherapy

    Zehao Wei1,#, Xuejian Liu2,#, Zheng Zhang1, Yimin Ma2,*, Min Xu1,*

    Oncology Research, Vol.34, No.7, 2026, DOI:10.32604/or.2026.078793 - 16 June 2026

    Abstract Pancreatic cancer is one of the most lethal malignancies, characterized by difficulties in early diagnosis, limited therapeutic options, and generally poor patient prognosis. In recent years, immunotherapy has provided new opportunities for the treatment of pancreatic cancer; however, its clinical efficacy has been substantially constrained by the complex tumor microenvironment (TME) and immune evasion mechanisms. With the rapid advancement of artificial intelligence (AI) technologies, AI has demonstrated great potential in the early detection of pancreatic cancer, prediction of immunotherapeutic responses, and design of personalized treatment strategies. This review systematically summarizes the latest advances in the More >

  • Open Access

    ARTICLE

    Progression-Free Survival with PARP Inhibitors According to Clinical Risk in Patients with Ovarian Cancer: An Indirect Comparison Using Reconstructed Data

    Lorenzo Gasperoni1,*, Luna Del Bono2, Alberto Farolfi3, Andrea Messori4,5, Vera Damuzzo5,6

    Oncology Research, Vol.34, No.7, 2026, DOI:10.32604/or.2026.077700 - 16 June 2026

    Abstract Background: Poly (ADP-ribose) polymerase (PARP) inhibitors (PARPi) are established maintenance treatments in ovarian cancer, but comparative efficacy across genetic profiles and relapse risk categories remains unclear. The aim of this study was to compare the efficacy of different PARPi as maintenance therapy in ovarian cancer across genetic profiles and relapse risk categories using reconstructed individual patient data (IPD) from randomized trials (RCTs). Methods: IPD were reconstructed using the IPDfromKM method from published Kaplan-Meier curves of RCTs stratified by clinical risk subgroup. Progression-free survival (PFS) was the primary endpoint. Three comparisons were performed: Breast Cancer gene (BRCA)+… More >

  • Open Access

    ARTICLE

    Exploring the Role of CD44 in the Progression and Invasion of Chondrosarcoma

    Zoe Bell1, Corey D. Chan1,2, Rachel Howarth3, Andrea Atkinson1, Zakareya Gamie1,4, Daniel Frankel5, Oana Bretcanu5, Kenneth S. Rankin1,2,*

    Oncology Research, Vol.34, No.7, 2026, DOI:10.32604/or.2026.075617 - 16 June 2026

    Abstract Objectives: Chondrosarcoma is the most common type of primary bone sarcoma in adults with a high risk of local recurrence and metastasis. Chondrosarcomas are largely resistant to chemotherapy and radiotherapy, meaning that surgery is the mainstay of treatment for most patients. Therefore, new therapeutic targets are required. Cluster of differentiation 44 (CD44) is a transmembrane protein that has roles in cell proliferation, adhesion and migration and is shown to be overexpressed in several cancer types. Consequently, this work was undertaken to understand whether CD44 could be a potential therapeutic target in chondrosarcoma. Methods: In this study,… More > Graphic Abstract

    Exploring the Role of CD44 in the Progression and Invasion of Chondrosarcoma

  • Open Access

    ARTICLE

    UCK2 Drives Lung Adenocarcinoma Progression and Immune Dysregulation via the RHEB/mTOR Signaling Axis

    Xiaolin Wei1,2, Jing Guo1, Chuntao Tao3, Yong Bao2, Li Yang1,*, Hong Chen1,*

    Oncology Research, Vol.34, No.6, 2026, DOI:10.32604/or.2026.078651 - 21 May 2026

    Abstract Objectives: Uridine-cytidine kinase 2 (UCK2) plays a crucial role in the pyrimidine salvage pathway, but its function in lung adenocarcinoma (LUAD) is still largely unclear. The study aimed to investigate the expression, prognostic value, biological functions, and molecular mechanisms of UCK2 in LUAD. Methods: Bioinformatic analyses were performed using The Cancer Genome Atlas (TCGA), Gene Set Cancer Analysis (GSCA), Gene Expression Omnibus (GEO), and Genotype Tissue Expression (GTEx) datasets. In vitro assays evaluated the effect of UCK2 overexpression on LUAD cells. Co-immunoprecipitation and pathway analyses were utilized to explore the underlying mechanism. Immune landscape and drug sensitivity… More >

  • Open Access

    ARTICLE

    Repurposing Artesunate to Combat Progression and Metastasis via Targeting Circulating Tumor Cells

    Evangelia Pantazaka1,#, Dimitrios Papakonstantinou1,#, Argyro Roumeliotou1, Dafni Graikioti2, Sotirios Tsakas1, Nefeli Zacharopoulou3, Stuart S. Martin4, Athanasios Kotsakis5, Constantinos M. Athanassopoulos2, Catherine Alix-Panabières6,7,8, Galatea Kallergi1,*

    Oncology Research, Vol.34, No.6, 2026, DOI:10.32604/or.2026.075600 - 21 May 2026

    Abstract Objectives: Circulating tumor cells (CTCs) drive metastasis and exhibit resistance to conventional therapies, making them crucial therapeutic targets. Artesunate (AS), a derivative of artemisinin, displays anticancer activity, including inhibition of JunB proto-oncogene (JUNB) and programmed death ligand-1 (PD-L1) and upregulation of Vimentin (VIM), markers related to poor prognosis in CTCs. This study aimed to evaluate the effects of AS on adherent and non-adherent cancer cell lines (breast, lung, colon), the patient-derived colon cancer CTC-MCC-41 line, and CTCs from small-cell lung cancer (SCLC) patients. Methods: AS’s effect was evaluated using TetherChip technology. Cell viability was measured using… More > Graphic Abstract

    Repurposing Artesunate to Combat Progression and Metastasis via Targeting Circulating Tumor Cells

  • Open Access

    ARTICLE

    Claudin-1 Interacts with CD81 and Promotes the Progression of Colorectal Cancer

    Kaidi Yin, Lili Deng, Wen Liu*

    Oncology Research, Vol.34, No.6, 2026, DOI:10.32604/or.2026.075185 - 21 May 2026

    Abstract Objectives: Although claudin-1 (CLDN1) interacts with Cluster of Differentiation 81 (CD81) in various cell types, the specific mechanism underlying this interaction and its functional implications in colorectal cancer (CRC) cells remain poorly understood. This study outlines the regulatory role of CLDN1 in CRC cell tumorigenicity through its interaction with CD81, elucidating the underlying signaling cascade. Methods: Changes in the expression of CLDN1 and CD81, as well as their correlation with the survival of CRC patients, were analyzed using samples from The Cancer Genome Atlas database, the Kaplan‒Meier plotter database, and tissue microarrays. CLDN1 and CD81 were… More >

  • Open Access

    RETRACTION

    Retraction: miR-122 Inhibits Hepatocarcinoma Cell Progression by Targeting LMNB2

    Oncology Research Editorial Office

    Oncology Research, Vol.34, No.5, 2026, DOI:10.32604/or.2026.081624 - 22 April 2026

    Abstract This article has no abstract. More >

  • Open Access

    ARTICLE

    SLC16A1 Activates the STAT3/SLC7A11 Pathway to Mediate Ferroptosis Resistance and Tumor Progression in Head and Neck Squamous Cell Carcinoma

    Chunhui Tian1,2, Weipin Xie1,2, Wen Li2, Huaiyu Gu2, Xuebao Liu2, Busheng Tong1,*, Yehai Liu1,*, Huaiyuan Zong3,*

    Oncology Research, Vol.34, No.5, 2026, DOI:10.32604/or.2026.077171 - 22 April 2026

    Abstract Background: In head and neck squamous cell carcinoma (HNSCC), solute carrier family 16 member 1 (SLC16A1) is associated with tumor advancement and reduced sensitivity to ferroptosis, yet the molecular basis of these effects remains unclear. This study seeks to uncover how SLC16A1 contributes to HNSCC tumorigenesis. Methods: To elucidate how SLC16A1 drives HNSCC progression via ferroptosis resistance, we performed RNA sequencing on SLC16A1-knockdown HNSCC cells and controls, followed by functional validation. We next systematically assessed the role of the candidate molecule solute carrier family 7 member 11 (SLC7A11) in HNSCC progression and resistance to ferroptosis… More > Graphic Abstract

    SLC16A1 Activates the STAT3/SLC7A11 Pathway to Mediate Ferroptosis Resistance and Tumor Progression in Head and Neck Squamous Cell Carcinoma

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