International journal of oncology最新文献

{"title":"PDLIM2 acts as a central regulator of ubiquitination, immune signaling, and mitochondrial metabolism in lung cancer suppression (Review).","authors":"Tsung-Hsien Chuang, Jeng-Hung Guo, Jing-Xing Yang, Jen-Chih Tseng, Hung-Jung Wang, Chao-Yang Lai","doi":"10.3892/ijo.2026.5909","DOIUrl":"10.3892/ijo.2026.5909","url":null,"abstract":"<p><p>Lung cancer is a leading cause of cancer‑related mortality worldwide, which underscores the need to identify novel targets for improving early detection, therapeutic efficacy, and long‑term patient outcomes. PDZ and LIM domain protein 2 (PDLIM2) is a multifunctional adaptor protein that plays a role in cancer biology, particularly in lung cancer. Although PDLIM2 exerts divergent functions across various cancer types, substantial clinical, genetic, and experimental evidence consistently supports its role as a tumor suppressor in lung cancer. PDLIM2 expression is markedly downregulated in the majority of lung tumors representing various histological subtypes and disease stages, and its loss is strongly associated with poor prognosis. Mechanistically, it functions as an E3 ubiquitin ligase or ubiquitin ligase enhancer to promote the degradation of key transcription factors, including NF‑κB/RelA and STAT3, thereby restraining tumor‑associated inflammation, proliferation, survival, immune evasion, and metabolic reprogramming. PDLIM2 downregulation in lung cancer occurs through coordinated genetic and epigenetic mechanisms, including loss of heterozygosity at chromosome 8p21, promoter hypermethylation, histone deacetylation, and oxidative stress‑driven transcriptional repression. Functionally, the restoration of PDLIM2 suppresses lung tumor growth, enhances chemosensitivity, and promotes antitumor immunity, including response to immune checkpoint inhibitors. In addition, a protumoral mechanism of PDLIM2 downregulation involves mitochondrial dysfunction and accumulation of oncometabolites that lead to the activation of hypoxia inducible factor‑1α signaling. Overall, PDLIM2 is emerging as a biomarker and therapeutic target for lung cancer management.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 2","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344301/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148375693","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] Downregulation of uPA/uPAR inhibits intermittent hypoxia‑induced epithelial‑mesenchymal transition (EMT) in DAOY and D283 medulloblastoma cells.","authors":"Reshu Gupta, Chandramu Chetty, Praveen Bhoopathi, Sajani Lakka, Sanjeeva Mohanam, Asti S Rao, Dzung H Dinh","doi":"10.3892/ijo.2026.5902","DOIUrl":"10.3892/ijo.2026.5902","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned reader drew to the Editor's attention that there were anomalies associated with the cellular images shown in Fig. 1A; essentially, groupings of cells/cellular features appeared to be strikingly similar in appearance, looking internally within four of the eight data panels in this figure. A similar phenomenon of strikingly similar features was observed in the majority of the panels showing spheroid formation assay data in Fig. 8A. Moreover, regarding the western blots shown in Fig. 2B for the D283 cell line, the protein bands shown for E‑cadherin for the normoxia and hypoxia cells [the (N) lanes] were strikingly similar, suggesting that the gels in this figure may have featured inappropriate editing. Finally, some of the western blot data featured in Fig. 5C were very similar to data that had appeared in a paper by the same authors published in the journal PLoS One. After having conducted an internal investigation of the data in this paper, the Editor of <i>International Journal of Oncology</i> has decided that this article should be retracted from the journal on the grounds of a lack of confidence in the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply.The Editor sincerely apologizes to the readership for any inconvenience caused, and we thank the reader for bringing this matter to our attention. [International Journal of Oncology 733‑744, 2011; DOI: 10.3892/ijo.2010.883].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 2","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148217468","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":"Radiotherapy resistance in glioblastoma: Mechanistic insights and novel therapeutic approaches (Review).","authors":"Dengtian Zhang, Yiming Zhang, Fen Liu, Cong Zhang, Shulong Jiang","doi":"10.3892/ijo.2026.5907","DOIUrl":"10.3892/ijo.2026.5907","url":null,"abstract":"<p><p>Glioblastoma (GBM) is currently the most lethal type of primary brain tumor, with a median survival time of 15‑20 months despite the use of multimodal therapy. Although radiotherapy (RT) remains a cornerstone of GBM treatment, a subset of patients who initially respond to RT eventually acquire resistance, leading to tumor relapse. The emergence of radioresistance severely impairs the long‑term efficacy of RT, highlighting the importance of understanding its underlying mechanisms. The present review synthesizes emerging evidence that therapy‑induced remodeling of the blood‑brain barrier (BBB), upregulation of ATP‑binding cassette efflux transporters, hypoxia‑driven hypoxia inducible factor‑1α signaling and tumor microtube (TM)‑mediated intercellular communication converge to create a self‑reinforcing resistance network. These interconnected mechanisms collectively drive adaptive radioresistance, rather than acting in isolation. Based on this framework, the present review evaluates therapeutic strategies designed to disrupt distinct nodes of this network, including epigenetic modulators, poly (ADP‑ribose) polymerase inhibitors, BBB‑penetrant agents and TM‑targeting approaches, such as connexin43 peptide inhibitors and high‑linear energy transfer particle therapy. The clinical implications of these findings are discussed, with emphasis on biomarker‑driven patient stratification and combinatorial regimens that concurrently target multiple resistance mechanisms.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 2","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13329789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338552","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] Honokiol, a phytochemical from <i>Magnolia spp.</i>, inhibits breast cancer cell migration by targeting nitric oxide and cyclooxygenase‑2.","authors":"Tripti Singh, Santosh K Katiyar","doi":"10.3892/ijo.2026.5904","DOIUrl":"10.3892/ijo.2026.5904","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the cell migration assay data shown in Fig. 2A on p. 772, the 'Honokiol Conc. 10 <i>µ</i>M' data panels relating to the 4T1 and MCF‑7 cell lines contained an overlapping section, such that data which were intended to show the results from experiments performed in different cell lines had been derived from the same original source. In addition, the western blot data featured in Fig. 4A were published at around the same time in a couple of papers in different journals that featured the same authors, wherein the experiments reported were conducted differently compared with the experimental conditions reported in the above paper; both of these papers have subsequently been retracted. Given the re‑use of data that has been identified in the above paper, together with the apparently incorrect assembly of the data in Fig. 2A, 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 38: 769‑776, 2011; DOI: 10.3892/ijo.2011.899].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 2","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338497","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] TIP60 governs the auto‑ubiquitination of UHRF1 through USP7 dissociation from the UHRF1/USP7 complex.","authors":"Tanveer Ahmad, Waseem Ashraf, Abdulkhaleg Ibrahim, Liliyana Zaayter, Christian D Muller, Ali Hamiche, Yves Mély, Christian Bronner, Marc Mousli","doi":"10.3892/ijo.2026.5908","DOIUrl":"10.3892/ijo.2026.5908","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the GAPDH control western blots shown in Fig. 5A on p. 9 for the experiments without MG132 treatment ('‑ MMGM132') were strikingly similar to the GAPDH control western blots shown in Fig. 5D, albeit with some horizontal and vertical resizing of the bands. In addition, an independent analysis of the data in this paper revealed that the flow cytometric plots for the TIP60‑transfected cells experiment in Fig. 8B on p. 12 were also strikingly similar to the plots shown to represent the TIP60‑eGFP Positive cells experiment in Fig. 8E. The authors have been contacted by the Editorial Office to offer an explanation for the apparent re‑use of the abovementioned data in this paper, and we are awaiting their response. 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 59: 89, 2021; DOI: 10.3892/ijo.2021.5269].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 2","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338550","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":"Understanding the epigenetic regulation of lactylation and aberrant lactate metabolism in cancer: From mechanisms to therapeutic strategies (Review).","authors":"Xiaoli Zheng, Jiayi Zhang, Chengwei Mao, Yingxue Si, Chengcheng Chi, Tingting Xiong, Mengjie Gu, Chunyan Zhang, Haiying Han, Yangling Li, Chong Zhang","doi":"10.3892/ijo.2026.5906","DOIUrl":"10.3892/ijo.2026.5906","url":null,"abstract":"<p><p>Tumor metabolic reprogramming is a hallmark of cancer, supporting adaptation to hostile microenvironments and sustained malignancy. Among these changes, abnormal lactate metabolism is central to tumor progression, immune evasion and therapy resistance. Lactate, once considered a mere glycolytic byproduct, also acts as a signaling molecule influencing cancer behavior. Epigenetic mechanisms, including DNA/RNA methylation, histone modifications and non‑coding RNAs, serve key roles in regulating lactate metabolism. Notably, lactylation, a novel post‑translational modification, links lactate metabolism with epigenetic control. The present review outlines the molecular basis of lactate dysregulation, its epigenetic control and its biological impact on cancer, and highlights emerging therapeutic strategies targeting lactate metabolism.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 2","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344303/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338527","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":"Unraveling the roles of fibroblast activation protein‑positive cancer‑associated fibroblasts in cancer: From mechanisms to therapy (Review).","authors":"Zhixin Tao, Zhuan Zhou, Yong Wu, Jinwei Hu","doi":"10.3892/ijo.2026.5903","DOIUrl":"10.3892/ijo.2026.5903","url":null,"abstract":"<p><p>Cancer‑associated fibroblasts (CAFs) in the tumor microenvironment (TME) are involved in tumor pathogenesis. Fibroblast activation protein (FAP)⁺ CAFs are the predominant CAF subtype across multiple cancer types, including breast, lung and pancreatic cancer. FAP⁺ CAFs are crucial contributors to tumor progression. However, incomplete understanding of the biology of FAP⁺ CAFs limits their potential for clinical application. The present review aimed to summarize the characteristic features, functions and underlying mechanisms of FAP⁺ CAFs in tumor growth, including their involvement in extracellular matrix organization, tumor expansion and immunomodulation within the TME, in which FAP plays an important role, and FAP⁺ CAF‑based strategies for tumor diagnosis and therapeutic intervention. The present study aimed to provide a conceptual framework for the multifaceted roles of FAP⁺ CAFs in cancer progression to guide development of optimized FAP⁺ CAF‑targeted diagnostics and therapies.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 2","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148277339","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":"Stress‑induced catecholamines attenuate sorafenib efficacy by inhibiting ferroptosis in β2‑adrenergic receptor positive renal cell carcinoma.","authors":"Masaki Ushijima, Sei Naito, Hiromi Ito, Takafumi Narisawa, Osamu Ichiyanagi, Hidenori Kanno, Hiroki Fukuhara, Yuki Takai, Mayu Yagi, Atushi Yamagishi, Hayato Nishida, Yutaro Obara, Norihiko Tsuchiya","doi":"10.3892/ijo.2026.5905","DOIUrl":"10.3892/ijo.2026.5905","url":null,"abstract":"<p><p>Ferroptosis, an iron‑dependent form of non‑apoptotic cell death, is a potential target for cancer therapy. Sorafenib, a molecular targeted agent for renal cell carcinoma (RCC), is involved in ferroptosis induction. Chronic stress, mediated by catecholamines via β2‑adrenergic receptors (ADRB2), promotes cancer progression, yet its influence on drug resistance and ferroptosis remains elusive. To investigate ADRB expression in RCC, immunohistochemistry of surgical specimens was performed and assessed ADRB mRNA and protein levels were assessed by RT‑qPCR and western blotting in RCC cell lines. To determine whether β‑adrenergic signaling modulates sorafenib sensitivity, we used ADRB2‑expresing ACHN cells and conducted MTS cell viability assays following β‑adrenergic agonist isoproterenol (ISO) stimulation, ADRB2 knockdown by siRNA, as well as a restraint‑stress mouse model in which catecholamine levels were elevated, bearing ACHN cells or ACHN cells with ADRB2 knockdown by shRNA. To evaluate the involvement of ferroptosis, we applied the ferroptosis inhibitor ferrostatin‑1 (Fer‑1) and inducers erastin and RSL3, and measured cell viability, malondialdehyde and reactive oxygen species. To elucidate the mechanism underlying the ISO effect on ferroptosis, MAPK pathway activity was assessed by western blotting and MTS assays performed under MAPK inhibition. The present study confirmed ADRB2 expression in RCC by immunohistochemistry of surgical specimens. Using the ADRB2‑expressing RCC cell line ACHN, the present study demonstrated that stimulation with the β‑adrenergic agonist isoproterenol (ISO) conferred resistance to sorafenib both <i>in vitro</i> and in a mouse stress model; this effect was abrogated by ADRB2 knockdown. Similarly to ISO, Fer‑1 diminished sorafenib sensitivity in ACHN cells. Erastin and RSL3 markedly decreased cell viability, however, ISO attenuated ferroptosis in ACHN cells. Mechanistically, ISO inhibited the phosphorylation of ERK1/2, p38 and JNK, all of which contribute to ferroptosis suppression. These findings provide evidence that chronic stress‑induced ADRB2 activation promotes sorafenib resistance by mitigating ferroptotic cell death.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 2","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148338499","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":"[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":"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":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186306/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P2X7 receptor: An emerging therapeutic target in acute myeloid leukemia (Review).","authors":"Yunqing Liu, Hongfan Xue, Hanheng Mai, Tan Sang, Zonghong Li, Na Wang, Lili Feng","doi":"10.3892/ijo.2026.5897","DOIUrl":"10.3892/ijo.2026.5897","url":null,"abstract":"<p><p>The P2X7 receptor (P2X7R) is a ligand‑gated ion channel that exhibits bifunctional properties, switching between a cation‑permeable channel and a large cytolytic pore. In acute myeloid leukemia (AML), P2X7R is aberrantly overexpressed, particularly in leukemia stem cells (LSCs) and AML blasts. Within the bone marrow niche of AML, P2X7R binding by extracellular adenosine triphosphate not only contributes to a profound immunosuppressive niche that protects the AML cells from immune surveillance, but also drives LSC proliferation, survival, homing, and self‑renewal through downstream signaling cascades, including the cAMP response element‑binding protein/phosphoglycerate dehydrogenase/serine metabolic axis, PBX homeobox 3, Wnt/β‑catenin, and c‑Myc. Elevated P2X7R expression is associated with poor prognosis, chemoresistance, and disease recurrence of AML. The central role of P2X7R in AML pathophysiology makes it a potential biomarker for prognostic stratification and a promising therapeutic target. Several targeting strategies are currently under investigation, including the small molecule antagonists and specific anti‑P2X7R antibodies. Furthermore, a therapeutic approach involves combining P2X7R inhibition with conventional chemotherapy. In conclusion, targeting the P2X7R pathway represents a potential novel and multi‑faceted strategy to improve outcomes for patients with AML by remodeling its protective microenvironment and directly attacking the leukemia cells.</p>","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/PMC13238206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054424","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}