International journal of oncology最新文献

{"title":"[Retracted] uPAR and cathepsin B knockdown inhibits radiation‑induced PKC integrated integrin signaling to the cytoskeleton of glioma‑initiating cells.","authors":"Kiranmai Alapati, Sreelatha Gopinath, Rama Rao Malla, Venkata Ramesh Dasari, Jasti S Rao","doi":"10.3892/ijo.2026.5844","DOIUrl":"10.3892/ijo.2026.5844","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, regarding the wound healing assay data shown in Fig. 2D, a pair of the data panels appeared to be overlapping, such that the data from the same original source had apparently been used to show the results of differently performed experiments. Furthermore, concerning the immunohistochemical data shown in Fig. 7A and C, similarly, two pairs of the data panels contained overlapping data, where the results of different experiments were intended to have been portrayed. Owing to the duplications of data that were identified in this paper, the Editor of <i>International Journal of Oncology</i> has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. 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 41: 599‑610, 2012; DOI: 10.3892/ijo.2012.1496].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 3","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12823055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145933315","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":"<p>Unveiling sex differences in pancreatic ductal adenocarcinoma: Current evidence and future directions (Review)</p>.","authors":"Sophie Rauschenberg, Elisabeth Orgler-Gasche, Didem Karakas Zeybek, Ivonne Regel, J-Matthias Löhr, Daniel Öhlund, Michael Günther, Lina Aguilera Munoz","doi":"10.3892/ijo.2026.5848","DOIUrl":"10.3892/ijo.2026.5848","url":null,"abstract":"<p><p><p>Pancreatic ductal adenocarcinoma (PDAC) is the seventh leading cause of cancer‑related death worldwide in both men and women. While sex‑specific differences are increasingly recognized as critical determinants of health and disease, particularly in oncology, they remain markedly underexplored in PDAC. Emerging evidence suggests that sex differences influence numerous aspects of PDAC, including treatment response and prognosis. This knowledge gap represents a notable barrier to the development of effective, personalized therapeutic strategies for both sexes. The present review provides a comprehensive overview of the current knowledge on sex‑based differences in PDAC, encompassing epidemiology, risk factors, chemotherapy pharmacokinetics and toxicity, prognosis, therapeutic response, immune interactions, tumor microenvironment, tumor microbiota and molecular biomarkers.</p>.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 3","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12823057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989205","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] LTBP2 promotes the migration and invasion of gastric cancer cells and predicts poor outcome of patients with gastric cancer","authors":"Jun Wang, Wen-Jia Liang, Guang-Tao Min, Hong-Peng Wang, Wei Chen, Nan Yao","doi":"10.3892/ijo.2026.5847","DOIUrl":"10.3892/ijo.2026.5847","url":null,"abstract":"<p><p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell migration and invasion assay data shown in Fig. 5A on p. 1895 were strikingly similar to data in an article written by different authors at different research institutes that had already been accepted for publication in the journal <i>OncoTargets and Therapy</i>. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>International Journal of Oncology</i>, the Editor 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 52: 1886‑1898, 2018; DOI: 10.3892/ijo.2018.4356]</p>.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 3","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12823058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989156","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":"PTPN18 functions as a tumor suppressor in breast cancer by negatively regulating cyclin E.","authors":"Na Zhang, Tao Wang, Bin Bai, Xiaonan Zhang, Wenying Xu, Weilu Chen, Yang Yu, Bing Wang","doi":"10.3892/ijo.2025.5843","DOIUrl":"10.3892/ijo.2025.5843","url":null,"abstract":"<p><p>Protein tyrosine phosphatase non‑receptor 18 (PTPN18) is widely expressed in breast cancer (BC) cell lines. Additionally, high levels of PTPN18 facilitate an improved overall survival and prognosis in patients with BC. However, the effects and mechanisms of PTPN18 in BC remain unclear. In the present study, it was found that PTPN18 serves a tumor suppressor role in BC cells by promoting apoptosis, inhibiting proliferation and metastasis and inducing cell cycle arrest. Bioinformatics analysis showed that PTPN18 was significantly negatively correlated with the cell cycle and downregulated cyclin E expression, which was consistent with the experimental results. Subsequent co‑immunoprecipitation assay results showed that PTPN18 could bind to cyclin E and promote its degradation through the ubiquitin‑proteasome pathway. Moreover, the addition of cyclin E2 did not reduce the binding of PTPN18 to cyclin E1. In the present study, the signaling pathways involved in cell cycle regulation were further investigated and it was found that PTPN18 may regulate the expression levels of cyclin‑dependent kinase (CDK) inhibitor 1A and CDK inhibitor 1B proteins through phosphatidylinositol 3‑kinase/protein kinase B signaling pathway, which leads to cell cycle arrest and tumor inhibition in BC. Thus, analysis of the tumor suppressor mechanism of PTPN18 not only helps us to understand its biological function but also provides a theoretical basis for the development of new therapeutic strategies for BC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 3","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12823060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889064","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":"<p>Circ72309 modulates gemcitabine metabolism and gemcitabine sensitivity in pancreatic cancer: Serum Circ72309 levels as a potential predictor of treatment response</p>.","authors":"Naoko Sekiguchi, Hidenori Takahashi, Shogo Kobayashi, Kazuki Sasaki, Shinichiro Hasegawa, Yoshifumi Iwagami, Daisaku Yamada, Yoshito Tomimaru, Hirofumi Akita, Tadafumi Asaoka, Takehiro Noda, Junzo Shimizu, Koji Tanaka, Ryota Chijimatsu, Yuichiro Doki, Hidetoshi Eguchi","doi":"10.3892/ijo.2026.5849","DOIUrl":"10.3892/ijo.2026.5849","url":null,"abstract":"<p><p><p>Circular RNAs (circRNAs) are associated with various biological features of cancer, including chemosensitivity and the structural characteristics of circRNAs indicate their potential as liquid biomarkers. Gemcitabine is a cornerstone treatment for pancreatic cancer (PC). A deeper understanding of gemcitabine sensitivity and the exploration of clinically valuable liquid biomarkers that are predictive of gemcitabine sensitivity may contribute to the development of improved‑tailored treatment strategies for PC. The aim of the present study was to identify a candidate circRNA associated with gemcitabine sensitivity, investigate its biological functions and evaluate its potential as a liquid biomarker in predicting gemcitabine sensitivity. circRNA sequencing analysis was conducted to identify candidate circRNAs and the function of a candidate circRNA in modulating gemcitabine sensitivity was investigated <i>in vitro</i>. Further, the potential of this circRNA in predicting gemcitabine sensitivity in patients with PC who received gemcitabine‑based neoadjuvant chemotherapy was evaluated using pre‑treatment serum samples. circ72309 was identified as the candidate circRNA and its overexpression in gemcitabine‑resistant PC cell lines increased gemcitabine‑induced apoptosis and markedly increased gemcitabine sensitivity <i>in vitro</i>. Furthermore, circ72309 decreased cytidine deaminase by increasing reactive oxygen species activity and increasing human equilibrative nucleoside transporter 1 expression via regulation of target miRNAs. Patients with high serum circ72309 had markedly improved progression‑free survival (PFS) and high serum circ72309 was an independent prognostic predictor of a favorable PFS in patients with PC. circ72309 affected multiple steps in the gemcitabine metabolic pathway and its overexpression resulted in markedly increased gemcitabine sensitivity. Therefore, circ72309 expression in the pre‑treatment serum samples may serve as a predictor of gemcitabine sensitivity in patients with PC.</p>.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 3","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12823056/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989174","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":"<p>Regulatory networks of HIFs in tumor‑infiltrating immune cells: From molecular mechanisms to therapeutic implications (Review)</p>.","authors":"Chaoqun Li, Chenge Qin, Xingchen Li, Jinzhu Wang, Yang Li, Qin Sun","doi":"10.3892/ijo.2026.5845","DOIUrl":"10.3892/ijo.2026.5845","url":null,"abstract":"<p><p><p>Hypoxic tumor microenvironment (TME) is a common occurrence in the development of solid tumors, which activates hypoxia‑inducible factors (HIFs) and their downstream signaling pathways in cancer cells to facilitate tumor progression and immune escape. However, among the various immune cells that constitute innate and adaptive immune systems, HIFs have a more intricate function; moreover, different isoforms of HIFs play different functions under spatial and temporal conditions. HIFs are conducive to the adaptation of various immune cells to the hypoxic TME. The stability of HIF‑α can regulate metabolism and directly regulate the expression of immune genes. Additionally, the activation of HIF signaling may also inhibit the development of immune cells in some tumor environments, affecting the antigen recognition and killing processes to assist cancer cells in immune escape. Therefore, understanding the relationship between HIF signaling and immune cells more comprehensively may yield substantial benefits for the immunotherapy of various types of cancer. The present study reviewed the role of HIFs in immunity, including their role in T cells, B cells, macrophages, neutrophils, dendritic cells and natural killer cells. It also discussed the effectiveness of HIF targeted therapy in clinical application, the challenges associated with it and the development of a precise targeting drug delivery system. The present review may help researchers comprehend the tumor immune process in a hypoxic microenvironment. It aimed to offer novel strategies for cancer immunotherapy and prolonging the overall survival of patients.</p>.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 3","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12823059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989121","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] Suppression of the death gene BIK is a critical factor for resistance to tamoxifen in MCF‑7 breast cancer cells.","authors":"Rubí Viedma-Rodriguez, Luis Arturo Baiza-Gutman, Alejandro García-Carrancá, Leticia Moreno-Fierros, Fabio Salamanca-Gómez, Diego Arenas-Aranda","doi":"10.3892/ijo.2025.5842","DOIUrl":"10.3892/ijo.2025.5842","url":null,"abstract":"<p><p>Following the publication of the above paper, a concerned reader drew to the Editor's attention that, in Fig. 6, the same data appeared to have been included in three of the flow cytometric plots featured in this figure (for the Non‑treated, Scrambled and SiRNAi BIK experiments). Moreover, the control β‑actin western blots in Figs. 2B, 4A and 8B appeared to be the same (although, in these cases, the lanes for the blots were labelled up identically, and so these apparent duplications may not have represented an incorrect assembly of these figures); similarly, the control blots in Fig. 7A and B were also matching. However, the control β‑actin western blots in three other figure parts (Fig. 1C and 7A/B) were also duplicated, and in this case, the numbers of lanes in the gel slices were different / the lanes were labelled differently. The authors were contacted by the Editorial Office to offer an explanation for these potential anomalies in the presentation of the data in this paper, although 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, the Editor of <i>International Journal of Oncology</i> has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 43: 1777‑1786, 2013; DOI: 10.3892/ijo.2013.2127].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 3","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12823054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145849874","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":"Roles of interleukins in spasmolytic polypeptide‑expressing metaplasia (Review).","authors":"Jiale Ma, Tiancheng Zhan, Xinyuan Zhang, Wang Gao, Shuangmei Zhao, Huizhen Li","doi":"10.3892/ijo.2025.5830","DOIUrl":"10.3892/ijo.2025.5830","url":null,"abstract":"<p><p>Gastric cancer (GC) is a major global health burden, ranking fifth in incidence and third in cancer‑related mortality. By 2040, there are expected to be ~1.8 million new cases and 1.3 million fatalities associated with GC. Spasmolytic polypeptide‑expressing metaplasia (SPEM) is a central component of gastric precancerous lesions, which remodels the gastric mucosa in response to injury through a lineage of mucus‑secreting cells. Interleukins (ILs) are the communication means for innate and adaptive immune cells as well as non‑immune cells and tissues. Their complex network regulation contributes to the development of SPEM and is a key driver in the transformation of SPEM to GC. The present review systematically described the IL‑related mechanisms underlying the formation and progression of SPEM and categorizes the roles of different ILs by family. In addition, the molecular association between IL dynamics and SPEM following <i>Helicobacter pylori </i>infection is explored, and various SPEM experimental model characteristics and IL‑based therapeutic strategy advances and limitations are discussed. The clinical translation of IL‑targeted therapies is limited, but the development of therapies that target pathogenesis specifically and the enhancement of IL therapy combinations with other therapeutic options may improve efficacy and reduce side effects. Increased understanding of the causes of SPEM and the mechanisms underlying GC may open up new avenues for early detection and targeted therapy.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 2","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12716909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145677599","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":"Targeted therapies for urothelial carcinoma: From FGFR inhibitors to next‑generation antibody-drug conjugates (Review).","authors":"Jinping Du, Hao Shen, Tongwei Zeng, Wei Liu, Yongqiang Xie","doi":"10.3892/ijo.2025.5841","DOIUrl":"10.3892/ijo.2025.5841","url":null,"abstract":"<p><p>Treatment of urothelial carcinoma (UC), particularly in metastatic or cisplatin‑ineligible patients, remains challenging because of limited durable responses to conventional chemotherapy and immune checkpoint inhibitors. Recent advances in targeted therapies, including FGFR inhibitors (for example, erdafitinib) and antibody‑drug conjugates (ADCs) targeting Nectin‑4 (enfortumab vedotin) and HER2 (disitamab vedotin), have reshaped treatment paradigms. FGFR3 alterations, which are present in 20‑40% of patients with advanced UC, predict sensitivity to FGFR tyrosine kinase inhibitors, whereas ADCs demonstrate efficacy across biomarker‑selected and unselected populations. However, clinical implementation is complicated by resistance mechanisms, such as kinase switching, phenotypic plasticity and tumor microenvironment interactions, as well as biomarker heterogeneity. The present review synthesizes current evidence on molecularly guided therapies, contrasts resistance mechanisms between FGFR inhibitors and ADCs, and evaluates strategies to overcome therapeutic limitations. By integrating translational insights and emerging preclinical data, it was aimed to provide a roadmap for optimizing biomarker‑driven approaches, novel combinations and next‑generation agents for the treatment of UC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 2","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12742833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145849904","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] Establishment and evaluation of a new highly metastatic tumor cell line 5a‑D‑Luc‑ZsGreen expressing both luciferase and green fluorescent protein.","authors":"Hitomi Sudo, Atsushi B Tsuji, Aya Sugyo, Hiroyuki Takuwa, Kazuto Masamoto, Yutaka Tomita, Norihiro Suzuki, Takeshi Imamura, Mitsuru Koizumi, Tsuneo Saga","doi":"10.3892/ijo.2025.5840","DOIUrl":"10.3892/ijo.2025.5840","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, regarding the bioluminescence and fluorescence images of the mouse shown in Fig. 2C and E respectively, the images/positioning of the mouse appeared to be unexpectedly similar, and the authors were asked to confirm whether the images were captured at the same time, but separate results were obtained for the luminescence and fluorescence readings. Similarly, in Fig. 3A, the same mouse image (re. its appearance and positioning) appeared to be shown for the 5a‑D‑Luc cell line on Days 14 and 28, albeit with different bioluminescence. Finally, upon analyzing the data independently in the Editorial Office, it came to light that, for the phase contrast images of the MDA‑MD‑231 and 5a‑D‑Luc cell lines shown in Fig. 1A, these appeared to be the same image, but with different lighting intensities and with the 5a‑D‑Luc image rotated through 90˚. The authors were contacted by the Editorial Office to offer an explanation for these possible anomalies in the presentation of the data in this paper, although 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 conitnues to investigate this matter further. [International Journal of Oncology 48: 525‑532, 2016; DOI: 10.3892/ijo.2015.3300].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 2","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12742832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145780985","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}