Oncology Research最新文献

{"title":"Efficacy of Immune Checkpoint Inhibitors in the Treatment for Head and Neck Cancer Patients: A Systematic Review and Network Meta-Analysis.","authors":"Jiao Li, Nurhayu Ab Rahman, Suharni Mohamad, Guang Yang, Caixia Zhao","doi":"10.32604/or.2025.065911","DOIUrl":"10.32604/or.2025.065911","url":null,"abstract":"<p><strong>Objectives: </strong>Checkpoint inhibitors have significantly improved outcomes in a number of malignancies. To determine the most effective course of treatment for head and neck squamous cell carcinoma (HNSCC), this systematic review evaluated the efficacy of several therapeutic approaches based on immune checkpoint inhibitors (ICIs).</p><p><strong>Methods: </strong>A comprehensive evaluation of the literature was conducted, looking at randomized controlled trials (RCTs) that were published in Embase, PubMed, and the Cochrane Central Register of Controlled Trials since database establishment. The risk of bias of the enrolled studies was analyzed using The Review Manager (RevMan) 5.4. Using network meta-analyses (NMA), the relative treatment effects on overall survival (OS) and progression-free survival (PFS) from qualifying randomized controlled trials were synthesized and evaluated.</p><p><strong>Results: </strong>Regarding OS, compared with nivolumab plus chemotherapy, chemotherapy (Hazard ratio (HR) = 2.1, 95% Confidence interval (CI): 1.2, 3.4) showed a treatment disadvantage. Meanwhile, nivolumab plus chemotherapy may represent the most efficient (57.89%) and has a lower cost among all the treatments enrolled in this study for advanced HNSCC. Regarding PFS, compared with nivolumab plus ipilimumab, nivolumab plus chemotherapy (HR = 0.4, 95% CI: 0.2, 0.8) showed treatment superiority. Additionally, nivolumab plus chemotherapy (77.18%) has the longest PFS among all interventions.</p><p><strong>Conclusion: </strong>Taking into account OS and PFS, the combination of nivolumab plus chemotherapy may appear to be the most effective option and is associated with a comparatively lower cost among all treatments included in this network meta-analysis, thereby recommending its use as a first-line therapy for HNSCC.</p><p><strong>Registration: </strong>INPLASY (2024070073).</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2263-2278"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015982","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":"First-Line Aumolertinib in <i>EGFR</i>-Mutant Advanced Non-Small Cell Lung Cancer: A Multicenter Real-World Retrospective Study with a Four-Year Follow-Up.","authors":"Xi Qin, Yulan Liu, Lin Zhu, Yunyan Mo, Jing Zhang, Zhuchun Jiang, Dongning Huang, Xinrong Hu, Jingzhang Li, Quanfang Chen, Feng Xue","doi":"10.32604/or.2025.064119","DOIUrl":"10.32604/or.2025.064119","url":null,"abstract":"<p><strong>Background: </strong>The use of third-generation different tyrosine kinase inhibitors (TKIs) is considered the most effective option for treating advanced non-small cell lung cancer (aNSCLC) with epidermal growth factor receptor (EGFR) mutations. However, there is limited information on the efficacy and safety of aumolertinib in patients remains these cases.</p><p><strong>Methods: </strong>The clinical records of patients receiving aumolertinib as first-line therapy across four hospitals in the Guangxi Zhuang Autonomous Region from April 2020 to December 2021 were retrospectively analyzed, using progression-free survival (PFS) as the primary endpoint and overall survival (OS) representing the secondary endpoint. Adverse events (AEs) were assessed using the Common Terminology Criteria for Adverse Events (CTCAE v5.0).</p><p><strong>Results: </strong>Approximately 47 patients with <i>EGFR</i>-Mutant aNSCLC were recruited, including 1 squamous cell carcinoma (SCC) patient, 1 <i>EGFR</i> G719C mutated patient, 1 <i>EGFR</i> S768 patient mutated, and 1 <i>EGFR</i> KDD mutated patient. The average follow-up duration was 48.1 months concluding in August 2024. The median PFS (mPFS) was 22.2 months (95% CI 17.6 to 26.7), while the median OS (mOS) was 39.7 months (95% CI 32.6 to 46.9). Patients with deletion of exon19 in <i>EGFR</i> (19del) showeda mPFS of 28.4 months, markedlylonger than those with the L858R point mutation (L858R), who had a mPFS of 15.2 months (<i>p</i> = 0.036). Overall, 22 patients (46.8%) had central nervous system (CNS) metastases at the basal level. The mPFS for this cohort was 19.7 months. Rashes (17.0%), skin decrustation (4.2%), pruritus (4.2%), dental ulcers (4.2%), increased creatine kinase (2.1%), and musculoskeletal pains (2.1%) were the most prevalent AEs in this study. Grade 3 and higher AEs were observed at a rate of 4.2%.</p><p><strong>Conclusion: </strong>This study concluded that aumolertinib has considerable safety and efficacy for <i>EGFR</i>-mutant NSCLC in a first-line defense.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2451-2462"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015938","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":"SORBS1 Knockdown Resists S/G2 Arrest and Apoptosis Caused by Polyphyllin H-Induced DNA Damage in Pancreatic Cancer.","authors":"Xinxin Hu, Yuye Xue, Fei Fang, Jie Li, Xiaofeng Yuan, Guang Cheng, Hailong Yuan, Yongqiang Zhang, Yuefei Zhou, Shuangwu Yang, Pengcheng Qiu, Yunyang Lu, Haifeng Tang","doi":"10.32604/or.2025.064454","DOIUrl":"10.32604/or.2025.064454","url":null,"abstract":"<p><strong>Objectives: </strong>The Sorbin and SH3 domain containing 1 (SORBS1), a protein linked to insulin signaling CBL interaction, was investigated for its role in pancreatic cancer apoptosis. This study explored polyphyllin H (PPH)'s ability to restore SORBS1-knockdown-mediated repair functions.</p><p><strong>Methods: </strong>PANC-1 cells were divided into Blank, overexpression (OE), and knockdown groups. CCK-8 assays assessed proliferation and drug toxicity. Western blot and flow cytometry analyzed SORBS1 levels and PPH effects. Comet assays quantified DNA damage. Subcutaneous xenograft tumors in nude mice (Blank vs. knockdown) were treated with PPH to evaluate <i>in vivo</i> efficacy. SORBS1-H2AX gene correlation was analyzed Spearman rank clustering (<i>p</i> < 0.05).</p><p><strong>Results: </strong>PPH suppressed pancreatic cancer growth <i>in vitro</i>/<i>vivo</i>, but its efficacy was attenuated by SORBS1 downregulation. Clinically, low SORBS1 correlated with poor prognosis. SORBS1 knockdown promoted tumor proliferation and reduced PPH-induced apoptosis. While PPH decreased tumor volume in both Blank and knockdown groups compared to controls, SORBS1 knockdown diminished PPH's inhibitory effects. Mechanistically, SORBS1 depletion mitigated PPH-triggered DNA damage, circumventing G2/M arrest by modulating WEE1, Cyclin A2, CDK1, and Cyclin B1, thereby impairing apoptosis.</p><p><strong>Conclusion: </strong>SORBS1 knockdown counteracts PPH-mediated S/G2 arrest and apoptosis by alleviating DNA damage in pancreatic cancer. These findings highlight SORBS1 as a critical modulator of PPH's therapeutic potential, linking its expression to chemoresistance mechanisms.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2491-2506"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408846/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015934","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":"<i>MYH11</i> Suppresses Colorectal Cancer Progression by Inhibiting Epithelial-Mesenchymal Transition via <i>ZEB1</i> Regulation.","authors":"Yuhang Jiang, Yijun Xu, Qi Zhu, Yingxia Wu, Zhe Wang, Shuang He, Shiyong Yu, Honggang Xiang","doi":"10.32604/or.2025.063501","DOIUrl":"10.32604/or.2025.063501","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is common and deadly, often leading to metastasis, challenging treatment, and poor outcomes. Understanding its molecular basis is crucial for developing effective therapies.</p><p><strong>Aims: </strong>This study aimed to investigate the role of Myosin Heavy Chain 11 (MYH11) in CRC progression, especially its effects on epithelial-mesenchymal transition (EMT) and cell behavior, and to explore its potential regulation by the EMT transcription factor zinc finger E-box binding homeobox 1 (ZEB1).</p><p><strong>Methods: </strong>Differential expression analysis was performed in the GSE123390 and TCGA-READ datasets, and 317 intersection genes were identified. The hub gene MYH11 was identified based on Protein-protein interaction (PPI) analysis and expression validation. The effects of MYH11 and the EMT transcription factor (ZEB1) on the behavior of CRC cells were investigated <i>in vitro</i>.</p><p><strong>Results: </strong>Bioinformatics research revealed that MYH11 was considerably downregulated in CRC samples as compared to normal samples. Overexpression of MYH11 inhibited the proliferation, migration, and invasion of CRC cells. Western blotting (WB) testing showed that MYH11 overexpression inhibited EMT by elevating E-cadherin levels while suppressing ZEB1, vimentin, and N-cadherin expressions. By contrast, overexpression of ZEB1 promoted EMT and enhanced migration, invasion, and proliferation of CRC cells. The negative impacts of MYH11 affecting EMT markers and cell behaviors were partially mitigated by co-overexpression of MYH11 and ZEB1, indicating that MYH11 regulates EMT and CRC progression through ZEB1.</p><p><strong>Conclusion: </strong>Our study shows MYH11 curbs CRC growth by blocking EMT and invasion, but ZEB1 overexpression reduces this effect. It uncovers key CRC pathways and suggests MYH11's therapeutic potential.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2379-2398"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015958","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":"ERRγ Promotes Multiple Myeloma Survival by Coordinating NF-κB Signaling and Mitochondrial Apoptosis Regulation.","authors":"Xiaobing Zhou, Ying Li, Zizi Jing, Wei Yu, Jianbin Chen","doi":"10.32604/or.2025.063700","DOIUrl":"10.32604/or.2025.063700","url":null,"abstract":"<p><strong>Background: </strong>Multiple myeloma (MM) remains a formidable clinical challenge due to its high relapse rate and resistance to existing therapies. Estrogen-related receptor gamma (ERRγ), a nuclear receptor critical for cellular energy metabolism, has been implicated in various cancers. but its role in MM remains unclear.</p><p><strong>Methods: </strong>ERRγ expression was assessed using bioinformatics and RT-qPCR. Functional studies were conducted through siRNA-mediated ERRγ knockdown and treatment with the inverse agonist GSK5182 to examine their effects on MM cell proliferation and apoptosis.</p><p><strong>Results: </strong>ERRγ was significantly upregulated in the bone marrow of MM patients, correlating with advanced clinical stages and pathological fractures. Inhibition of ERRγ reduced MM cell expansion both <i>in vitro</i> and <i>in vivo</i>, while promoting mitochondrial-dependent apoptosis. Co-immunoprecipitation assays demonstrated a physical association between ERRγ and P65. Inhibition of ERRγ attenuated canonical nuclear factor-kappa B (NF-κB) signaling by blocking the nuclear translocation of its key effector p65. Additionally, modulation of ERRγ altered receptor activator of nuclear factor-κB ligand (RANKL) levels, implying a potential role in bone degradation observed in MM cases.</p><p><strong>Conclusion: </strong>Collectively, the data broaden understanding of ERRγ's contribution to MM development and propose it as a viable target for therapeutic intervention.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2399-2420"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015962","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":"Pyrimethamine Inhibits Human Ovarian Cancer by Triggering Lethal Mitophagy via Activating the p38/JNK/ERK Pathway.","authors":"Lingjuan Linghu, Hongying Zhou, Gang Zheng, Tao Yi","doi":"10.32604/or.2025.063724","DOIUrl":"10.32604/or.2025.063724","url":null,"abstract":"<p><strong>Objectives: </strong>Ovarian cancer, a leading cause of gynecological malignancy-related mortality, is characterized by limited therapeutic options and a poor prognosis. Although pyrimethamine has emerged as a promising candidate demonstrating efficacy in treating various tumors, the precise mechanisms of its antitumor effects remain obscure. This study was specifically designed to investigate the mode of action underlying the antitumor effects of pyrimethamine in preclinical settings.</p><p><strong>Methods: </strong>The effects of pyrimethamine on cellular proliferation were meticulously assessed using both the cell counting kit 8 (CCK-8) assay and the colony formation assay, with the effects further confirmed in a murine model. A confocal microscope was utilized to monitor the dynamic alterations in mitochondria within ovarian cancer cells. Additionally, adenosine triphosphate (ATP) and reactive oxygen species (ROS) assays were conducted to measure mitochondrial damage induced by pyrimethamine in ovarian cancer cell lines. The mitochondrial membrane potential was assessed using fluorescent dyes as an indicator of mitochondrial functional status. Furthermore, transcriptome analysis and immunohistochemical techniques were employed to detect the impact of pyrimethamine on ovarian cancer cells.</p><p><strong>Results: </strong>Our results demonstrated that pyrimethamine induced ovarian cancer cell death through mitochondrial dysfunction and lethal mitophagy. Transcriptome profiling analysis and Western blot demonstrated that activation of the p38/JNK/ERK signaling pathway was implicated in the process of pyrimethamine-induced mitophagy in ovarian cancer cells. Importantly, combination treatment with pyrimethamine and paclitaxel <i>in vitro</i> and <i>in vivo</i> showed a synergistic antitumor effect.</p><p><strong>Conclusions: </strong>Altogether, these findings indicate that the antitumor effects of pyrimethamine result from the induction of lethal mitophagy via regulation of the p38/JNK/ERK pathway in ovarian cancer. Considering the low toxicity and high tolerance associated with pyrimethamine, it is suggested that pyrimethamine be evaluated in the treatment of ovarian cancer, either as a monotherapy or in combination with paclitaxel.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2421-2434"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015987","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":"Association among Noncoding-RNAs, APRO Family Proteins, and Gut Microbiota in the Development of Breast Cancer.","authors":"Akari Fukumoto, Satoru Matsuda","doi":"10.32604/or.2025.062810","DOIUrl":"10.32604/or.2025.062810","url":null,"abstract":"<p><p>The non-coding RNAs (ncRNAs) are a family of single-stranded RNAs that have become recognized as crucial gene expression regulators in normal and cancer cell biology. The gut microbiota, which consists of several different bacteria, can actively contribute to the regulation of host metabolism, immunity, and inflammation. Roles of ncRNAs and gut microbiota could significantly interact with each other to regulate the growth of various types of cancer. In particular, a causal relationship among ncRNAs, gut microbiota, and immune cells has been shown for their potential importance in the development of breast cancer. Alteration of ncRNA expression and/or gut microbiota profiles could also influence several intracellular signaling pathways with the function of anti-proliferative (APRO) family proteins associated with the malignancy. Targeting ncRNAs and/or APRO family proteins for the treatment of various cancers has been revealed with novel immune therapies. Here, the most recent studies to underline the key role of ncRNAs, APRO family proteins, and gut microbiota in breast cancer progression have been discussed. For more effective breast cancer therapy, it would be imperative to figure out the collective mechanism of ncRNAs, APRO family proteins, and gut microbiota.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2205-2219"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015989","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":"Combining Chemotherapeutic Agents, Targeted Therapies, Vaccines and Natural Bioactive Compounds for Mesothelioma: Advances and Perspectives.","authors":"Raffaele Carrano, Carlotta Zucca, Nicla Cristina, Martina Grande, Eleonora Leti Maggio, Riccardo Bei, Antonio Infante, Chiara Focaccetti, Valeria Lucarini, Loredana Cifaldi, Laura Masuelli, Luciano Mutti, Camilla Palumbo, Monica Benvenuto, Roberto Bei","doi":"10.32604/or.2025.066708","DOIUrl":"10.32604/or.2025.066708","url":null,"abstract":"<p><p>Mesothelioma is a rare and aggressive cancer with a poor prognosis and limited therapeutic options. Despite recent advances, conventional treatment approaches remain largely ineffective due to late diagnosis, chemoresistance and immunosuppressive tumor microenvironment. This review reports the latest studies on combination therapies for mesothelioma, focusing on the potential of integrating chemotherapeutic agents, molecularly targeted agents, vaccines and natural bioactive compounds such as polyphenols. Clinical and preclinical studies demonstrate that integrating immune-modulating drugs or molecular inhibitors with chemotherapy can improve survival and reduce tumor progression in mesothelioma models and patients. Vaccine-based strategies show potential for inducing host-persistent immune responses when combined with conventional treatments. Moreover, natural compounds such as polyphenols show synergistic effects with chemotherapeutics and targeted agents by modulating several signaling pathways involved in cancer cell growth and progression and by overcoming drug resistance. While several combination strategies are under clinical investigation, further studies are needed to develop more effective and personalized therapeutic approaches that could be translated into standardized treatment protocols.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2181-2204"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015991","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":"Advances in Tumor Microenvironment and Immunotherapeutic Strategies for Hepatocellular Carcinoma.","authors":"Jiahao Xue, Jingchang Zhang, Gang Chen, Liucui Chen, Xinjun Lu","doi":"10.32604/or.2025.063719","DOIUrl":"10.32604/or.2025.063719","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a highly aggressive malignancy, largely driven by an immunosuppressive tumor microenvironment (TME) that facilitates tumor growth, immune escape, and resistance to therapy. Although immunotherapy-particularly immune checkpoint inhibitors (ICIs)-has transformed the therapeutic landscape by restoring T cell-mediated anti-tumor responses, their clinical benefit as monotherapy remains suboptimal. This limitation is primarily attributed to immunosuppressive components within the TME, including tumor-associated macrophages, regulatory T cells (Tregs), and myeloid-derived suppressor cells (MDSCs). To address these challenges, combination strategies have been explored, such as dual checkpoint blockade targeting programmed cell death protein 1 (PD-1), programmed death-ligand 1 (PD-L1), and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), as well as synergistic use of ICIs with anti-angiogenic agents or TME-targeted interventions. These approaches have shown encouraging potential in enhancing immune efficacy. This review outlines the complex crosstalk between the TME and immunotherapeutic responses in HCC, emphasizing how combination regimens may overcome immune resistance. Furthermore, we discuss the remaining hurdles, including therapeutic resistance and immune-related adverse events, and propose future directions involving TME-associated biomarkers and individualized treatment strategies to improve patient outcomes.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2309-2329"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015931","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":"Emerging HER2 Targeting Immunotherapy for Cholangiocarcinoma.","authors":"Prin Sungwan, Jutatip Panaampon, Ratchaneewan Sumankan, Genki Aoki, Seiji Okada","doi":"10.32604/or.2025.065319","DOIUrl":"10.32604/or.2025.065319","url":null,"abstract":"<p><p>Cholangiocarcinoma (CCA) is a fatal bile duct malignancy. CCA is intrinsically resistant to standard chemotherapy, responds poorly to it, and has a poor prognosis. Effective treatments for cholangiocarcinoma remain elusive, and a breakthrough in CCA treatment is still awaited. The human epidermal growth factor receptor 2 (HER2) plays an oncogenic role by promoting an aggressive cancer phenotype through multiple pathways. While HER2 has shown increasing potential as an effective target for breast and gastric cancers over the last decade, this has not been the case for CCA. This review explores the possibility of targeting HER2 in CCA immunotherapy. Key findings suggest that HER2 alterations have been reported as one of the signatures associated with a poorer prognosis in liver fluke-associated CCA, the most prevalent subtype in Southeast Asia. Furthermore, we assess recent advances in HER2-targeted therapeutic approaches, presenting the current stage, rationale, and evidence supporting the use of HER2 as a promising therapeutic target for cancer immunotherapy in CCA. We also emphasize the crucial role of animal models in developing anticancer therapies. In summary, focusing on HER2 expression could provide alternative strategies for the HER2-altered CCA cluster.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 9","pages":"2279-2307"},"PeriodicalIF":4.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015936","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}