International journal of oncology最新文献_第7页

[Corrigendum] Cell density‑dependent regulation of p73 in breast cancer cells. [勘误]乳腺癌细胞中p73的细胞密度依赖性调控。

IF 7.3 3区医学

International journal of oncology Pub Date : 2026-07-01 Epub Date: 2026-05-29 DOI: 10.3892/ijo.2026.5898

Chaitali Tophkhane, Shihe Yang, Zhizhuang Joe Zhao, Xiaohe Yang

{"title":"[Corrigendum] Cell density‑dependent regulation of p73 in breast cancer cells.","authors":"Chaitali Tophkhane, Shihe Yang, Zhizhuang Joe Zhao, Xiaohe Yang","doi":"10.3892/ijo.2026.5898","DOIUrl":"10.3892/ijo.2026.5898","url":null,"abstract":"Subsequently to the publication of the above article, an interested reader drew to the authors' attention that the control β‑actin blots shown for the western blots portrayed in Figs. 1B and 2B were strikingly similar after a slight adjustment was made to one set of the bands, even though the experiments shown for the p73β protein were different in these figure parts. After re‑examining their original data, the authors have realized that the β‑actin blots correctly shown for Fig. 2B had inadvertently been included in Fig. 1B. The revised version of Fig. 1, now showing the β‑actin blots that were correctly associated with Fig. 1B, is shown opposite. The authors are grateful to the Editor of International Journal of Oncology for allowing them this opportunity to publish a Corrigendum, and all the authors agree to its publication. Note that this error did not grossly affect either the results or the conclusions reported in this study; furthermore, the authors apologize to the readership for any inconvenience caused. [International Journal of Oncology 35: 1429‑1434, 2009; DOI: 10.3892/ijo_00000461].","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 1","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13238208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054454","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}

引用次数: 0

METTL3 in esophageal cancer: Current insights into molecular mechanisms, subtype heterogeneity and targeted therapy prospects (Review). METTL3在食管癌中的分子机制、亚型异质性和靶向治疗前景（综述）

IF 7.3 3区医学

International journal of oncology Pub Date : 2026-06-01 Epub Date: 2026-04-24 DOI: 10.3892/ijo.2026.5884

Chunlan Pu, Huan Hu, Hengrui Fan, Tao Chen, Jiao Tang

{"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":"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.","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":7.3,"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}

引用次数: 0

Novel therapeutic strategies for metastatic castration‑resistant prostate cancer: Beyond androgen receptor pathway inhibition (Review). 转移性去势抵抗性前列腺癌的新治疗策略：超越雄激素受体途径抑制（综述）。

IF 7.3 3区医学

International journal of oncology Pub Date : 2026-06-01 Epub Date: 2026-04-17 DOI: 10.3892/ijo.2026.5882

Yaqin Wang, Yongqiang Xie, Qiang Zhao

{"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":"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.","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":7.3,"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}

引用次数: 0

Biomarkers for oesophageal squamous cell carcinoma and the role of HPV: Multi‑omics approaches and current evidence (Review). 食管鳞状细胞癌的生物标志物和HPV的作用：多组学方法和当前证据（综述）。

IF 7.3 3区医学

International journal of oncology Pub Date : 2026-06-01 Epub Date: 2026-04-24 DOI: 10.3892/ijo.2026.5887

Limin Zou, Hongzhou Zhao, Jiaying Zhang, Jialing Xie, Xiaolu An, Xianhua Qi, Yuting Yue, Lijia Zhang, Xiajun Zhang, Kuancan Liu

{"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":"10.3892/ijo.2026.5887","url":null,"abstract":"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.","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":7.3,"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}

引用次数: 0

Research advances in aptamers in the diagnosis and treatment of breast cancer (Review). 适配体在乳腺癌诊断和治疗中的研究进展（综述）。

IF 7.3 3区医学

International journal of oncology Pub Date : 2026-06-01 Epub Date: 2026-04-24 DOI: 10.3892/ijo.2026.5885

Liqiang Chu, Yunfeng Xiao, Xinhua Li, Jiawei Cui, Luyao Ma, Bin Shao, Hongwei Cui

{"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":"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.","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":7.3,"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}

引用次数: 0

[Retracted] MicroRNA‑155 promotes tumor growth of human hepatocellular carcinoma by targeting ARID2. 【撤回】MicroRNA‑155通过靶向ARID2促进人肝细胞癌的肿瘤生长

IF 7.3 3区医学

International journal of oncology Pub Date : 2026-06-01 Epub Date: 2026-04-24 DOI: 10.3892/ijo.2026.5886

Li Zhang, Wei Wang, Xiaobin Li, Sai He, Jianfeng Yao, Xiaolong Wang, Di Zhang, Xuejun Sun

{"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":"10.3892/ijo.2026.5886","url":null,"abstract":"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 International Journal of Oncology 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 International Journal of Oncology 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].","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":7.3,"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}

引用次数: 0

RRP9 suppresses hepatocellular carcinoma progression by inhibiting the PI3K/AKT/mTOR pathway. RRP9通过抑制PI3K/AKT/mTOR通路抑制肝癌进展。

IF 7.3 3区医学

International journal of oncology Pub Date : 2026-06-01 Epub Date: 2026-04-09 DOI: 10.3892/ijo.2026.5880

Zhengkang Fu, Man Li, Keshuai Dong, Jiarui Feng, Weixing Wang

{"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":"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.","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":7.3,"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}

引用次数: 0

[Expression of Concern] AHIF promotes glioblastoma progression and radioresistance via exosomes. [关注表达]AHIF通过外泌体促进胶质母细胞瘤的进展和放射耐药。

IF 7.3 3区医学

International journal of oncology Pub Date : 2026-06-01 Epub Date: 2026-04-17 DOI: 10.3892/ijo.2026.5883

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

引用次数: 0

[Retracted] Antitumor activity of NRC‑AN‑019 in a pre‑clinical breast cancer model. NRC - AN - 019在临床前乳腺癌模型中的抗肿瘤活性

IF 7.3 3区医学

International journal of oncology Pub Date : 2026-06-01 Epub Date: 2026-04-03 DOI: 10.3892/ijo.2026.5879

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

引用次数: 0

[Corrigendum] PRIMA‑1 inhibits growth of breast cancer cells by re‑activating mutant p53 protein. [勘误]PRIMA‑1通过重新激活突变型p53蛋白抑制乳腺癌细胞的生长。

IF 7.3 3区医学

International journal of oncology Pub Date : 2026-06-01 Epub Date: 2026-04-09 DOI: 10.3892/ijo.2026.5881

Yayun Liang, Cynthia Besch-Williford, Salman M Hyder

{"title":"[Corrigendum] PRIMA‑1 inhibits growth of breast cancer cells by re‑activating mutant p53 protein.","authors":"Yayun Liang, Cynthia Besch-Williford, Salman M Hyder","doi":"10.3892/ijo.2026.5881","DOIUrl":"10.3892/ijo.2026.5881","url":null,"abstract":"Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, regarding the immunohistochemical images shown in Fig. 1B on p. 1018, the 'PAb1620/PM 25μM' and 'PAb1620/PM 50μM' data panels shown in Fig. 1B for the T47‑D and HCC‑1428 cell lines were apparently the same, sugggesting that this figure had been assembled incorrectly. After re‑examining their original data, the authors have realized that the 'PAb1620/PM 25μM' and 'PAb1620/PM 50μM' data panels correctly shown for the T47‑D cell line had inadvertently been copied across for the HCC‑1428 cell line. The revised version of Fig. 1, now showing all the correct data for the HCC‑1428 cell line in Fig. 1B, is shown below. The authors are grateful to the Editor of International Journal of Oncology for allowing them this opportunity to publish a Corrigendum, and all the authors agree to its publication. Note that this error did not grossly affect either the results or the conclusions reported in this study; furthermore, the authors apologize to the readership for any inconvenience caused. [International Journal of Oncology 35: 1015‑1023, 2009; DOI: 10.3892/ijo_00000416].","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 6","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638799","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}

引用次数: 0