Oncology reports最新文献

{"title":"PRMT7 at the crossroads of cancer progression and therapeutic targeting (Review).","authors":"Yuchen He, Jiayi Lou, Yijing Huang, Wen Deng, Xuehong Cai","doi":"10.3892/or.2026.9208","DOIUrl":"https://doi.org/10.3892/or.2026.9208","url":null,"abstract":"<p><p>Protein arginine methyltransferase 7 (PRMT7), the sole type III PRMT family member, catalyzes arginine monomethylation and has recently emerged as an important regulator of cancer biology. Increasing evidence indicates that PRMT7 participates in tumor initiation and progression through epigenetic regulation, transcriptional control, RNA processing and signaling pathway modulation. Dysregulated PRMT7 expression has been reported in diverse malignancies, including leukemia, breast cancer, lung cancer, renal cell carcinoma, hepatocellular carcinoma, prostate cancer and gastric cancer. Functionally, PRMT7 has been implicated in epithelial‑mesenchymal transition, cancer stemness, metastasis and immune modulation, although its effects may vary depending on cellular and tumor context. The present review summarizes the structural and biochemical features of PRMT7, its mechanistic roles across different cancer types, and its potential as a therapeutic target. Recent progress in PRMT inhibitor development was also discussed, with particular emphasis on PRMT7‑selective compounds such as SGC3027, SGC8158 and JS1310, as well as the key challenges that remain for clinical translation. Elucidating the context‑specific functions and targetable vulnerabilities of PRMT7 may provide new opportunities for precision cancer therapy.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 6","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Expression of Concern] ZNF703 promotes tumor cell proliferation and invasion and predicts poor prognosis in patients with colorectal cancer.","authors":"Feng Ma, Lihong Bi, Gongli Yang, Mengnan Zhang, Cuiping Liu, Yingying Zhao, Yadong Wang, Jide Wang, Yang Bai, Yali Zhang","doi":"10.3892/or.2026.9205","DOIUrl":"10.3892/or.2026.9205","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned reader has contacted the Editorial Office to draw attention to the fact that there appeared to be discrepancies between the numbers of patients reported with low‑ or high‑ZNF703 expression in Fig. 3 on p. 1074: Fig. 3A reported 70 patients with low ZNF703 expression and 68 patients with high expression; however, the stage‑stratified Kaplan‑Meier  curves showed the following: In Fig. 3B, stages I‑IIIA: 57 low‑expression and 20 high‑expression patients, and in Fig. 3C, stages IIIB‑IV: 20 low‑expression and 41 high‑expression patients (and so 70 vs. 68 patients in Fig. 3A, and 77 vs. 61 patients in Fig. 3B and C). In addition, the AJCC stage‑specific counts reported in Table I also showed internal inconsistencies in terms of the overall numbers of low‑ and high‑expression patients, and finally, an additional discrepancy was noted for the definition of the high expression group: The Materials and methods section stated that an immunohistochemical score of ≥6 was classified as high expression, whereas the Table I column heading defined high expression as '>6'. To clarify these apparent discrepancies, the authors should resolve the following: i) provide the actual numbers of low‑ and high‑expression patients in each AJCC stage group; ii) clarify whether the cutoff used for the Kaplan‑Meier analyses was ≥6 or >6; iii) provide the exact patient numbers used to generate Fig. 3A, B and C; and iv) clarify whether the counts, totals and percentages in Table I require correction. Finally, upon performing an independent analysis of the data in this paper in the Editorial Office, it came to light that, regarding the wound healing assay data shown in Fig. 6A on p. 1076, the '24 h / Control' and '24 h / NC siRNA' panels showed an overlapping section of data, such that data which were intended to show the results of experiments performed under different conditions had apparently been derived from the same original source. The authors have been contacted by the Editorial Office to offer an explanation for the apparent anomalies in the description of the data, and the incorrect assembly of data in Fig. 6, in this paper, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of this potential issue concerning the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Oncology Reports 32: 1071‑1077, 2014; DOI: 10.3892/or.2014.3313].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 6","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13659731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 neoadjuvant therapy for locally advanced head and neck squamous cell carcinoma (Review).","authors":"Hong You, Xinghu Qin, Shaozhi Fu","doi":"10.3892/or.2026.9210","DOIUrl":"https://doi.org/10.3892/or.2026.9210","url":null,"abstract":"<p><p>The majority of head and neck cancers arise from the mucosal squamous epithelium of the oral cavity, pharynx and larynx, and are collectively referred to as head and neck squamous cell carcinoma (HNSCC). A multimodal standard of care is applied for case management. Primary oral cavity cancers are treated with resection followed by adjuvant cisplatin‑based chemoradiotherapy (CRT), and definitive concurrent CRT is applied for pharyngeal or laryngeal disease. In human papillomavirus‑negative patients who are medically unfit for platinum treatment, the epidermal growth factor receptor‑directed monoclonal antibody cetuximab is administered concomitantly with radiotherapy (RT). More recently, immune checkpoint inhibitors (ICIs) have redefined systemic therapy for recurrent/metastatic HNSCC, yielding durable responses and a survival benefit. In total, 65‑70% of patients present with stage III‑IVA locally advanced (LA) disease, a scenario associated with therapeutic challenges and a marked deterioration in the quality of life. Neoadjuvant therapy is designed to downstage the primary tumor, eradicate occult micrometastatic disease and enhance locoregional control before definitive surgery or RT, thus offering a rational strategy for organ preservation. Contemporary regimens integrate taxane, platinum and 5‑fluorouracil induction chemotherapy with RT, and early‑phase trials have explored the feasibility and efficacy of incorporating ICIs into neoadjuvant protocols. The present review summarizes the evolution of neoadjuvant therapy for LA HNSCC, with particular emphasis on emerging immunotherapy‑based paradigms and their potential to improve oncological and functional outcomes.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 6","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PBRM1 knockdown is associated with NRF2‑dependent ALDOA upregulation and metabolic reprogramming in HCCC‑9810 intrahepatic cholangiocarcinoma cells.","authors":"Dong Zhang, Dezheng Liu, Shukuan Yang, Zijian Zhao, Xuekai Zhao, Yongshuo Liu, Fan Zhang, Lei Zhou","doi":"10.3892/or.2026.9212","DOIUrl":"https://doi.org/10.3892/or.2026.9212","url":null,"abstract":"<p><p>Polybromo‑1 (PBRM1) is a chromatin‑remodeling factor that is altered in intrahepatic cholangiocarcinoma (ICC). The present study examined the effects of PBRM1 knockdown on tumor‑related phenotypes and glucose metabolism in HCCC‑9810 ICC cells. The present study also evaluated the roles of aldolase, fructose‑bisphosphate A (ALDOA) and nuclear factor erythroid 2‑related factor 2 (NRF2). Publicly available ICC mutation data were analyzed descriptively. The present study evaluated HCCC‑9810 cells following PBRM1 knockdown using proliferation, colony formation, wound‑healing, Transwell, metabolic, reverse transcription‑quantitative PCR, western blotting, apoptosis and mitochondrial membrane‑potential assays. ALDOA and NRF2 perturbation experiments were used to examine their contribution to the PBRM1‑knockdown phenotype. HCCC‑9810‑derived xenografts were used for <i>in vivo</i> assessment. PBRM1 knockdown increased proliferation, migration and invasion in HCCC‑9810 cells and altered several glucose‑metabolism readouts. ALDOA expression also increased following PBRM1 knockdown. ALDOA silencing attenuated several metabolic and survival‑related changes. NRF2 overexpression increased ALDOA expression, whereas NRF2 knockdown reduced it. Co‑silencing NRF2 attenuated the ALDOA increase associated with PBRM1 knockdown. In xenografts, PBRM1 knockdown was associated with greater tumor growth, higher ALDOA expression and a higher Ki67 signal. PBRM1 knockdown was associated with a tumor‑promoting metabolic phenotype in HCCC‑9810 cells, with ALDOA contributing to several metabolic and survival‑related changes. NRF2 perturbation further supported an NRF2‑dependent component of ALDOA regulation in this HCCC‑9810 model; however, the upstream mechanism responsible for increased NRF2 after PBRM1 knockdown remains unresolved. These findings warrant validation in independent ICC models.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 6","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CHCHD2 as a prognostic biomarker and therapeutic target in lung adenocarcinoma: Insights from pan‑cancer multi‑omics and functional studies.","authors":"Zikai Xu, Jie Shen, Yizhou Lin, Haotian Shi, Cong Zhang, Zhengwei Zhang, Xiaoyu Zhou, Zheng Yang","doi":"10.3892/or.2026.9213","DOIUrl":"https://doi.org/10.3892/or.2026.9213","url":null,"abstract":"<p><p>Lung adenocarcinoma (LUAD) remains a leading cause of cancer‑related mortality, and mitochondrial proteins have been increasingly implicated in tumor progression. Coiled‑coil‑helix‑coiled‑coil‑helix domain‑containing 2 (CHCHD2) has been reported in several malignancies, yet its pan‑cancer landscape and LUAD‑specific functional relevance have not been comprehensively evaluated. In the present study, multi‑omics analyses were integrated using The Cancer Genome Atlas‑derived datasets and public resources [including Gene Expression Profiling Interactive Analysis (GEPIA) 2, CIBERSORT and CellMiner] to characterize CHCHD2 expression patterns, clinical associations, tumor microenvironment (TME) features, stemness‑related indices and drug‑response correlations across cancers, followed by experimental validation in LUAD models. CHCHD2 was found to be upregulated in multiple cancers and was correlated with advanced disease stage and poor overall survival, especially in patients with LUAD. CHCHD2 promoted cell proliferation and migration while inhibiting apoptosis. CHCHD2 knockdown reduced AKT and ERK phosphorylation and suppressed xenograft tumor growth <i>in vivo</i>. High CHCHD2 expression was associated with increased stemness, an immunosuppressive TME, and differential drug‑response patterns in CellMiner analyses, suggesting that CHCHD2 expression may be associated with compound‑specific sensitivity profiles. Collectively, these findings support an oncogenic role of CHCHD2 in LUAD and highlight its potential utility as a prognostic biomarker and therapeutic target.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 6","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SEC31A promotes gastric cancer progression by inducing the PI3K/AKT/mTOR pathway and enhancing the CCL5‑mediated M2 polarization and recruitment of tumor‑associated macrophages.","authors":"Xixian Zhao, Liuye Huang","doi":"10.3892/or.2026.9211","DOIUrl":"https://doi.org/10.3892/or.2026.9211","url":null,"abstract":"<p><p>SEC31 homolog A (SEC31A) is associated with a variety of cancers. This study elucidated the role of SEC31A in gastric cancer (GC). The expression of SEC31A in GC was analyzed using western blotting and immunohistochemistry. Functional experiments were performed to detect the impact of SEC31A on GC proliferation, migration and invasion. The PI3K inhibitor LY294002 was used to explore the regulation of the biological functions by SEC31A through the PI3K/AKT/mTOR pathway in GC cells. Co‑culture of THP‑1 (human leukemia cell line of monocytic origin) and GC cells was conducted to investigate the impact of SEC31A on the M2 macrophage polarization in tumor immune microenvironment. Our investigation observed elevated expression of SEC31A in both GC tissue and cell lines. Through functional studies, suppression of SEC31A was found to decrease epithelial‑mesenchymal transition (EMT), proliferation, migration and invasion in GC cells. Overexpression of SEC31A led to activation of the PI3K/AKT/mTOR signaling cascade. The PI3K inhibitor LY294002 counteracted the increases in proliferation, migration, invasion and EMT triggered by SEC31A. Co‑culture experiments involving THP‑1 and GC cells indicated that SEC31A enhanced the recruitment and M2 polarization of macrophages via CCL5 within the GC tumor microenvironment (ME). To assess the influence of M2 macrophages on malignant behavior of GC cells, M2 macrophage‑conditioned medium (M2‑CM) was applied. M2‑CM mitigated the inhibitory effects on malignant phenotypes in GC cells following SEC31A knockdown. Moreover, diminished SEC31A expression enhanced the efficacy of anti‑PD‑1 therapy in GC models. Collectively, SEC31A promoted GC progression via activating the PI3K/AKT/mTOR pathway and facilitating CCL5‑mediated M2 polarization and recruitment of tumor‑associated macrophages. SEC31A knockdown may augment the anti‑tumor response to anti‑PD‑1 treatment in GC. These findings highlight SEC31A as a valuable prognostic indicator and potential target for immunotherapy in GC, offering novel strategies to enhance the effectiveness of anti‑PD‑1 therapy.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 6","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR‑324‑5p in oncology: Molecular mechanisms and clinical outlook (Review).","authors":"Kun Zhang, Zhen Xu, Yan Bin Luo, Chao Qi Liu, Yong Qin Zhou","doi":"10.3892/or.2026.9209","DOIUrl":"https://doi.org/10.3892/or.2026.9209","url":null,"abstract":"<p><p>MicroRNAs (miRNAs or miRs) represent a class of regulatory non‑coding RNAs that control post‑transcriptional gene expression and influence multiple cancer‑associated biological processes. Among these molecules, miR‑324‑5p exhibits cancer type‑dependent functions, displaying tumor‑suppressive activity in certain types of malignancy while promoting oncogenic phenotypes in others. The molecular basis responsible for these opposing effects remains to be fully clarified. The present review summarizes evidence and integrates pan‑cancer analyses from The Cancer Genome Atlas to characterize the molecular mechanisms of miR‑324‑5p across different types of malignancies, with emphasis on experimental findings from animal models investigating tumor growth and metastasis. The clinical relevance of miR‑324‑5p, including its diagnostic, prognostic and therapeutic implications, is also discussed, together with challenges limiting clinical translation, particularly tumor‑specific delivery strategies and <i>in vivo</i> stability. Further elucidation of the molecular contexts governing miR‑324‑5p activity may facilitate its application in precision oncology.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 6","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] miR‑29a inhibits human retinoblastoma progression by targeting STAT3.","authors":"Shu Liu, Xiaomeng Zhang, Chunmei Hu, Yingxue Wang, Chunling Xu","doi":"10.3892/or.2026.9207","DOIUrl":"https://doi.org/10.3892/or.2026.9207","url":null,"abstract":"<p><p>Following the publication of this paper, and a corrigendum (doi: 10.3892/or.2017.6144) published in 2021 to take account of duplicated western blot data that were identified in Fig. 4D, it has subsequently come to light that flow cytometric plots featured in Fig. 2D and Transwell invasion assay data in Fig. 3B, both on p. 742, contained data that were strikingly similar to data that had already been published in articles written by different research groups at different research institutes in a number of different journals. Given that the contentious data named above had already been published prior to the receipt of this paper at <i>Oncology Reports</i>, the Editor has decided that this paper should now be retracted from the Journal. After contacting the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 39: 739‑746, 2018; DOI: 10.3892/or.2017.6144].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 6","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of V‑domain Ig suppressor of T cell activation in ovarian cancer and its regulation of follicular regulatory T‑cell function via the AKT/MAPK pathway.","authors":"Yan Ma, Yidan Xu, Chunxia Yu, Huatuo Wu, Li Li","doi":"10.3892/or.2026.9206","DOIUrl":"https://doi.org/10.3892/or.2026.9206","url":null,"abstract":"<p><p>The high mortality associated with ovarian cancer is closely linked to immune remodeling within the tumor microenvironment (TME). V‑domain Ig suppressor of T cell activation (VISTA), a novel immune checkpoint, has attracted increasing attention in tumor immunology; however, its effects on follicular regulatory T (Tfr) cell function remain unclear. The present study examined VISTA expression in ovarian cancer and explored the correlation between VISTA and alterations in the AKT/MAPK pathway in Tfr‑like cells. Ovarian cancer tissues from different clinical stages and non‑malignant control tissues were analyzed by immunofluorescence, reverse transcription‑quantitative PCR and western blotting to assess VISTA expression and its association with FOXP3⁺CXCR5⁺ Tfr‑like cell infiltration. Naive CD4⁺ T cells were differentiated into Tfr‑like cells <i>in vitro</i>, and VISTA overexpression and silencing models were used to evaluate cell proliferation, cytokine secretion, and AKT/MAPK pathway activation. VISTA expression increased with ovarian cancer progression and was positively associated with Tfr‑like cell infiltration. <i>In vitro</i>, VISTA promoted Tfr‑like cell proliferation and the secretion of the anti‑inflammatory cytokines interleukin‑10 and transforming growth factor beta 1 while suppressing the immune effector molecules interleukin‑21 and granzyme B, accompanied by reduced AKT and extracellular signal‑regulated kinase 1/2 phosphorylation. Collectively, VISTA is upregulated in ovarian cancer and changes in VISTA expression are associated with enhanced immunosuppressive function of Tfr‑like cells as well as altered AKT/MAPK phosphorylation levels. These findings provided new insights into the regulation of the ovarian cancer TME and support further investigation of VISTA‑targeted immunotherapy.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 6","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overcoming melanoma drug resistance: Mechanisms and clinical progress of oncolytic viruses combined with immune checkpoint inhibitors (Review).","authors":"Yuan He, Wenxuan Lin, Haofang Chen, Yongqi Guan, Congcong Guan, Yanxiang Zhang, Dongsheng Pan","doi":"10.3892/or.2026.9197","DOIUrl":"10.3892/or.2026.9197","url":null,"abstract":"<p><p>Although immune checkpoint inhibitors (ICIs) have revolutionized the management of advanced melanoma, a major clinical challenge persists: Nearly 50% of patients develop primary or acquired resistance and therefore derive no meaningful clinical benefit. As ICIs are increasingly used in earlier disease settings, including adjuvant and neoadjuvant therapy, the population of patients with ICI‑resistant disease continues to grow. For patients whose disease progresses after first‑line combined programmed cell death 1 (PD‑1) and cytotoxic T‑lymphocyte associated protein 4 (CTLA‑4) blockade, effective salvage options remain limited, highlighting an urgent unmet medical need. Oncolytic viruses (OVs), which exert antitumor effects through the dual mechanisms of selective tumor cell lysis and immunomodulatory remodeling of the tumor microenvironment, represent a compelling therapeutic strategy for overcoming ICI resistance. Recent clinical and preclinical advances have moved OV‑ICI combination regimens from conceptual strategies to clinically evaluable interventions for refractory melanoma. Nevertheless, several translational barriers impede their broader implementation, including interpatient heterogeneity in treatment response, uncertainty regarding the optimal sequencing and dosing of combination therapies, and the lack of validated predictive biomarkers. The present review systematically synthesizes emerging clinical evidence and mechanistic insights into OV‑ICI synergy to inform rational trial design, refine combination strategies, and accelerate the development of precision immuno‑oncology approaches.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 5","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613317/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}