International journal of oncology最新文献

{"title":"[Corrigendum] Tumor necrosis factor‑α triggers opposing signals in head and neck squamous cell carcinoma and induces apoptosis via mitochondrial‑ and non‑mitochondrial‑dependent pathways.","authors":"Denis Selimovic, Renate U Wahl, Emmanuelle Ruiz, Rizwan Aslam, Thomas W Flanagan, Sofie-Yasmin Hassan, Simeon Santourlidis, Youssef Haikel, Paul Friedlander, Mosaad Megahed, Emad Kandil, Mohamed Hassan","doi":"10.3892/ijo.2026.5888","DOIUrl":"https://doi.org/10.3892/ijo.2026.5888","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the Editor's attention that a number of western blots in the paper appeared to contain incorrectly assembled data. First, comparing the F. Length (full‑length) Caspase 3 blots in Fig. 1F with the p‑ASK1 blots in Fig. 2C revealed that they were remarkably similar after horizontally flipping one set of the bands. In addition, the cytochrome c (Cyt. C) bands in Fig. 1F were similarly found to be remarkably similar to the IκBα blots in Fig. 2A, again after horizontal flipping of one set of the bands. Finally, it was noted that the β‑actin bands in Fig. 5C were very similar to the blots included in Fig. 3B to show the Tom20 data. After having examined the raw data underling these figures (which were also presented to the Editorial Office for our inspection), the authors realized that data in Figs. 1, 2, 3 and 5 were inadvertently assembled incorrectly in these figures. The revised versions of Figs. 1, 2, 3 and 5 are shown on the subsequent six pages. Specifically, in Fig. 1F, the blot for Cyt. C was incorrectly chosen; in Fig. 2A, the blot for IkBα was incorrectly chosen; in Fig. 3B, the blot for Tom20 was incorrectly chosen; and in Fig. 5C, the β‑actin blots shown to represent the gels for both the treated and control CLS‑354 and RPMI 2650 cells were incorrectly placed in this figure. These data have all been replaced with the correct data in the figures shown subsequently in this Corrigendum. The authors regret that the errors in Figs. 1F, 2A, 2C, 3B and 5C went unnoticed in the published versions of these figures in this paper, although note that these errors did not influence either the validity of the published data or the conclusions described in the article. The authors are grateful to the Editor of <i>International Journal of Oncology</i> for allowing them the opportunity to publish this Corrigendum. All the authors agree with the publication of this Corrigendum, and apologize to the readership for any inconvenience caused. [International Journal of Oncology 55: 1324‑1338, 2019; DOI: 10.3892/ijo.2019.4900].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770854","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":"Circulating proteins as biomarkers of response to cancer immunotherapy (Review).","authors":"Celeste Pinard, Angeline Ginzac, Catherine Abrial, Xavier Durando, Nina Radosevic-Robin","doi":"10.3892/ijo.2026.5889","DOIUrl":"https://doi.org/10.3892/ijo.2026.5889","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) have revolutionized cancer management; however, durable benefit is observed only in a minority of patients. To overcome the limitations of currently approved tumour tissue‑based biomarkers of response, several approaches based on liquid biopsy are currently being developed. Among them, circulating proteins, such as soluble immune checkpoint regulators, cytokines, chemokines, growth factors and cellular modulators, are being increasingly assessed by multiplex technologies that use a low volume of biofluids and offer rapid results. Serum/plasma programmed death‑ligand 1, cytotoxic t‑lymphocyte‑associated protein 4, T‑cell immunoglobulin and mucin‑domain containing‑3, lymphocyte activation gene‑3, interleukin (IL)‑6 and IL‑8 have emerged as potentially useful indicators of early response or resistance to ICIs, particularly when quantified during treatment. However, the optimal timing of on‑treatment blood sampling remains to be determined. The current review aimed to present the most important findings on the association between circulating proteins and response to ICIs in solid tumours, and to discuss the position of this biomarker class in the current landscape of biomarkers for ICI therapy.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837685","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":"METTL3 in esophageal cancer: Current insights into molecular mechanisms, subtype heterogeneity and targeted therapy prospects (Review).","authors":"Chunlan Pu, Huan Hu, Hengrui Fan, Tao Chen, Jiao Tang","doi":"10.3892/ijo.2026.5884","DOIUrl":"10.3892/ijo.2026.5884","url":null,"abstract":"<p><p>Esophageal cancer (EC), comprising esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC), urgently requires novel targeted therapies. The m⁶A methyltransferase METTL3 has emerged as a critical epitranscriptomic regulator in gastrointestinal malignancies. In ESCC, METTL3 functions predominantly as an oncogene, driving tumor progression via m⁶A‑dependent modulation of RNA stability, splicing, and translation across key networks, including NOTCH1, EGR1/Snail and Wnt/β‑catenin. Conversely, hypotheses regarding m⁶A‑independent functions or direct immune‑checkpoint regulation remain unvalidated in EC. Crucially, METTL3 actively modulates DNA damage repair and radiotherapy resistance, exposing a promising therapeutic vulnerability, although clinical pharmacological development remains nascent. Furthermore, METTL3 biology in EAC remains conspicuously uncharacterized. By strictly stratifying evidence by EC subtype, the present review distinguishes empirically validated mechanisms from premature cross‑cancer extrapolations. Ultimately, a novel conceptual framework that redefines METTL3 not merely as a static oncogene, but as a dynamic, context‑dependent regulatory hub, is proposed. Under therapeutic stress, METTL3 amplifies cellular phenotypic plasticity, systematically orchestrating tumor adaptation and treatment resistance.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124136/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770922","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":"Novel therapeutic strategies for metastatic castration‑resistant prostate cancer: Beyond androgen receptor pathway inhibition (Review).","authors":"Yaqin Wang, Yongqiang Xie, Qiang Zhao","doi":"10.3892/ijo.2026.5882","DOIUrl":"10.3892/ijo.2026.5882","url":null,"abstract":"<p><p>Metastatic castration‑resistant prostate cancer (mCRPC) remains a lethal disease due to universal resistance to androgen‑receptor pathway inhibitors (ARPI). Tumor progression is orchestrated by a spectrum of androgen‑receptor‑independent drivers, including genomic alterations in DNA damage repair pathways, epigenetic shifts promoting lineage plasticity, metabolic adaptations and an immunosuppressive tumor microenvironment. This evolving understanding has catalyzed the development of novel therapeutic strategies. These include PARP inhibitors for tumors with homologous recombination repair deficiencies, protein kinase B inhibitors for the phosphatase and tensin homolog‑loss subset, prostate‑specific membrane antigen (PSMA)‑targeted radioligand therapy, bispecific T‑cell engagers, antibody‑drug conjugates and immune checkpoint inhibitors. Furthermore, liquid biopsy profiling, PSMA‑positron emission tomography‑based radiomics and artificial intelligence platforms are enhancing real‑time patient selection and response assessment. The present review synthesized these recent preclinical and clinical advances to delineate biomarker‑driven, mechanism‑based therapeutic sequencing and combination strategies for mCRPC in the post‑ARPI era.19.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147698668","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":"Biomarkers for oesophageal squamous cell carcinoma and the role of HPV: Multi‑omics approaches and current evidence (Review).","authors":"Limin Zou, Hongzhou Zhao, Jiaying Zhang, Jialing Xie, Xiaolu An, Xianhua Qi, Yuting Yue, Lijia Zhang, Xiajun Zhang, Kuancan Liu","doi":"10.3892/ijo.2026.5887","DOIUrl":"https://doi.org/10.3892/ijo.2026.5887","url":null,"abstract":"<p><p>Oesophageal squamous cell carcinoma (ESCC) represents a major global health burden, particularly in regions with high incidence rates, significantly affecting patient quality of life and survival outcomes. Recent advances in multi‑omics technologies have highlighted their potential in identifying prognostic markers for ESCC. Concurrently, the possible association between human papillomavirus (HPV) infection and ESCC development has been investigated, although epidemiological evidence remains heterogeneous and a definitive causal role has not been universally established. This narrative review examines the progress in multi‑omics approaches for identifying prognostic markers of ESCC and provides a comprehensive analysis of the latest developments in HPV detection methods. Research from genomic, transcriptomic, proteomic, epigenomic, metabolomic, and immunomic studies was synthesized highlighting both promising biomarkers and the significant heterogeneity in reported results, particularly regarding HPV prevalence rates across various geographical regions and detection methods. The research included not only offers novel insights into the pathogenesis of ESCC but also lays a theoretical foundation for early diagnosis and personalized treatment; however, most findings remain investigational and require prospective validation before clinical implementation. The clinical implications and future research directions are discussed with consideration of current limitations.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770944","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":"Research advances in aptamers in the diagnosis and treatment of breast cancer (Review).","authors":"Liqiang Chu, Yunfeng Xiao, Xinhua Li, Jiawei Cui, Luyao Ma, Bin Shao, Hongwei Cui","doi":"10.3892/ijo.2026.5885","DOIUrl":"10.3892/ijo.2026.5885","url":null,"abstract":"<p><p>Cancer is a malignant disease that threatens human life and health. Among cancer types, breast cancer is one of the most common malignant tumors in women worldwide and ranks among the top cancer types in terms of incidence rate of malignant tumors in Chinese women. Aptamers are a class of DNA or RNA sequences that can bind to specific targets through their three‑dimensional structures, and are screened and obtained via systematic evolution of ligands by exponential enrichment technology. Aptamers have advantages of high affinity and specificity, strong stability, low immunogenicity, a wide range of targets and ease of preparation and purification. As effective molecular targeting tools and drug delivery carriers, aptamers and their conjugates show therapeutic potential in the early diagnosis and treatment of breast cancer. The present article reviewed the properties and screening techniques of aptamers, as well as their applications and research progress in the diagnosis and treatment of breast cancer, with the aim of providing new strategies and directions for the realization of precision medicine for breast cancer via aptamers.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124140/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770947","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":"[Retracted] MicroRNA‑155 promotes tumor growth of human hepatocellular carcinoma by targeting ARID2.","authors":"Li Zhang, Wei Wang, Xiaobin Li, Sai He, Jianfeng Yao, Xiaolong Wang, Di Zhang, Xuejun Sun","doi":"10.3892/ijo.2026.5886","DOIUrl":"https://doi.org/10.3892/ijo.2026.5886","url":null,"abstract":"<p><p>Following the publication of the above paper, a concerned reader drew to the Editor's attention that, in addition to concerns about the description of one of the antibodies employed in this study, the immunohistochemical data shown in Fig. 4E on p. 2429 and western blot data shown in Fig. 6E on p. 2431 had apparently appeared in figures in other papers that had already been submitted to the journals Oncotarget and <i>International Journal of Oncology</i> respectively, both of which were written by different authors at different research institutes. Upon performing an independent analysis of the data in the Editorial Office, we were able to validate these concerns; moreover, some of the same western blot data had also apparently been included in Figs. 4 and 5. Given that the abovementioned data had already been submitted for publication to other journals, the Editor of <i>International Journal of Oncology</i> has decided that this article should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 48: 2425‑2434, 2016; DOI: 10.3892/ijo.2016.3465].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124134/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770730","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":"RRP9 suppresses hepatocellular carcinoma progression by inhibiting the PI3K/AKT/mTOR pathway.","authors":"Zhengkang Fu, Man Li, Keshuai Dong, Jiarui Feng, Weixing Wang","doi":"10.3892/ijo.2026.5880","DOIUrl":"10.3892/ijo.2026.5880","url":null,"abstract":"<p><p>Ribosomal RNA processing 9 (RRP9) encodes a WD‑repeat domain‑containing protein, which is a potential carcinogenic biomarker for various tumors. As a key structural component of small nucleolar ribonucleoproteins, RRP9 serves a key role in ribosome biogenesis by facilitating 18S rRNA processing. Despite its association with the pathogenesis of various malignancies, its function and molecular mechanisms in hepatocellular carcinoma (HCC) remain unknown. The present study aimed to examine the biological role of RRP9 in HCC progression and the underlying regulatory mechanisms. Immunohistochemical and western blot analyses revealed a significant downregulation of RRP9 expression in patients with HCC compared with matched adjacent non‑tumorous tissues. To investigate RRP9 biological functions in HCC, stable RRP9‑knockdown and ‑overexpressing isogenic HCC cell line models were established using lentiviral transduction and puromycin selection. Functional assays, including Cell Counting Kit‑8 viability, colony formation, wound healing migration and Transwell invasion experiments, consistently demonstrated that RRP9 significantly suppressed HCC cell viability, proliferation, invasion and migration. Transcriptome sequencing and western blot analyses indicated that RRP9 inhibited the PI3K/AKT/mTOR pathway. Furthermore, functional rescue assays using the PI3K activator 740 Y‑P and the inhibitor PI3K/AKT/mTOR‑IN‑2 verified that RRP9 exerts its tumor‑suppressive role via this pathway. Protein‑protein interaction analysis revealed an association between RRP9 and cyclin A2 (CCNA2). Western blotting confirmed that RRP9 downregulated CCNA2 expression. Additionally, subcutaneous tumorigenesis in mice showed that RRP9 inhibits liver cancer progression via the PI3K/AKT/mTOR signaling pathway.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638854","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":"[Expression of Concern] AHIF promotes glioblastoma progression and radioresistance via exosomes.","authors":"Xuejun Dai, Keman Liao, Zhijun Zhuang, Binghong Chen, Zhiyi Zhou, Sunhai Zhou, Guoshi Lin, Feifei Zhang, Yingying Lin, Yifeng Miao, Zhiqiang Li, Renhua Huang, Yongming Qiu, Ruisheng Lin","doi":"10.3892/ijo.2026.5883","DOIUrl":"10.3892/ijo.2026.5883","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 2E on p. 264, the Transwell invasion assay results shown in the \"T98G‑AHIF KD\" data panel appeared to potentially contain an overlapping section with the \"U251‑AHIF OE\" data panel in Fig. 3E.  The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding 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. [International Journal of Oncology 54: 261‑270, 2019; DOI: 10.3892/ijo.2018.4621].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124142/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147698759","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":"[Retracted] Antitumor activity of NRC‑AN‑019 in a pre‑clinical breast cancer model.","authors":"Christopher S Gondi, Bharathi Gorantla, A K S Bhujanga Rao, K Amala, M U R Naidu, K V Jogi, G Venkat Ramana, Praveen C Myneni, Ajit Junnarkar, Jasti S Rao","doi":"10.3892/ijo.2026.5879","DOIUrl":"10.3892/ijo.2026.5879","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the 'Control' tumor images shown in Fig. 6A on p. 647 were unexpectedly similar to the tumor images shown five rows down for the 30 mg/kg Lapatinib administration experiment, albeit the images were turned through 180°. Owing to the fact that this figure appeared to have been assembled erroneously, and that data may have been duplicated within the figure to show the results of apparently different experiments, the Editor of <i>International Journal of Oncology</i> has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 39: 641‑648, 2011; DOI: 10.3892/ijo.2011.1079].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608641","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}