International journal of oncology最新文献

{"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":"<p><p>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 <i>International Journal of Oncology</i> 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].</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/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}

{"title":"Hypoxia‑induced exosomal CAMTA1 promotes radio‑resistance in MDA‑MB‑231 cells by regulating NRG1 to mediate M2 macrophage polarization.","authors":"Qian Li, Minghua Jiang, Biqing Zhu, Wei Wei, Lei Xia, Jian Huang, Han Gao, Mingyu Du","doi":"10.3892/ijo.2026.5875","DOIUrl":"10.3892/ijo.2026.5875","url":null,"abstract":"<p><p>Radiotherapy remains an irreplaceable treatment modality for breast cancer (BC). Calmodulin‑binding Transcription Activator 1 (CAMTA1) has been implicated in tumor progression; however, its role in BC is unclear. The present study aimed to elucidate the mechanistic function of CAMTA1 in BC. RNA sequencing was performed on RAW264.7 macrophages co‑cultured with 4T1 cells and subjected to X‑ray irradiation. <i>In vitro</i>, THP‑1 cells were co‑cultured with MDA‑MB‑231 cells under hypoxic conditions. Exosome morphology was observed under transmission electron microscopy and PKH67 staining was used to trace exosome uptake. Flow cytometry was used to detect CD163 expression while ELISA measured the levels of IL‑10 and IL‑12. Reverse transcription‑quantitative (RT‑q) PCR and immunoblotting analysis were used to detect the expressions of neuregulin 1 (NRG1), CAMTA1 and hypoxia‑inducible factor‑1α. Cell apoptosis, cell cycle distribution, cell viability and proliferation were evaluated using flow cytometry, MTT assay and colony formation assay. <i>In vivo</i>, transfected MDA‑MB‑231 cells were injected into BALB/c nude mice combined with radiotherapy and exosome injection. Histopathological changes in tumor tissues were examined using H&E staining. Immunohistochemistry analysis was performed to assess the expressions of NRG1, Caspase‑3 and CD163. RNA sequencing, RT‑qPCR and immunoblotting analysis revealed that NRG1 expression was markedly increased in RAW264.7 macrophages co‑cultured with 4T1 cells. NRG1 was found to be involved in M2 polarization induced by hypoxia‑treated MDA‑MB‑231 cells, which in turn promoted radio‑resistance. CAMTA1 expression was highly expressed in exosomes derived from hypoxic MDA‑MB‑231 cells and exosomal CAMTA1 promoted the M2 polarization of THP‑1 macrophages. <i>In vivo</i>, CAMTA1 overexpression greatly enhanced tumor growth, increased NRG1 expression, inhibited cell apoptosis and promoted M2 polarization of macrophages in tumor tissue. MDA‑MB‑231 cells were found to deliver CAMTA1 to macrophages via exosomes, leading to upregulation of NRG1 and induction of M2 polarization, thereby enhancing BC cells resistance to radiotherapy. These findings provided novel insights into the mechanisms underlying radio‑resistance in BC and identify exosomal CAMTA1 as a potential therapeutic target.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13038339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147529158","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] Epithelial protein lost in neoplasm‑α (EPLIN‑α) is a potential prognostic marker for the progression of epithelial ovarian cancer.","authors":"Rong Liu, Tracey A Martin, Nicola J Jordan, Fiona Ruge, Lin Ye, Wen G Jiang","doi":"10.3892/ijo.2026.5874","DOIUrl":"10.3892/ijo.2026.5874","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that, regarding the cell invasion assay experiments shown in Fig. 5A on p. 2493, the 'WT' and 'pEF6' data panels were strikingly similar, albeit the coloration of the images differed slightly from each other, suggesting that these images were derived from the same original source. A second reader also noted that, concerning the scratch‑wound assay experiments shown in Fig. 6B, the images for the WT and pEF6 experiments at the 0 h (top panels) and 36 h (lower panels) time points contained overlapping sections (specifically, the 'WT/0 h' panel with the pEF6/0 h panel, and the 'WT/36 h' panel with the pEF6/36 h panel), suggesting that the two pairs of panels were likewise derived from the same original sources. Upon examining their original data, the authors realized that these figures had been inadvertently assembled incorrectly. Revised versions of Figs. 5 and 6, now showing the correct data for the 'WT' panel in Fig. 5A and the pEF/0 h and pEF/36 h panels in Fig. 6B, are shown on the next two pages. Note that the errors made in assembling these figures did not have a gross effect on the conclusions reported in this study. The authors thank the Editor of <i>International Journal of Oncology</i> for granting them the opportunity to publish this corrigendum. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 48: 2488‑2496, 2016; DOI: 10.3892/ijo.2016.3462].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13038335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147485927","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] Influence of MLH1 on colon cancer sensitivity to poly(ADP‑ribose) polymerase inhibitor combined with irinotecan.","authors":"Lucio Tentori, Carlo Leonetti, Alessia Muzi, Annalisa Susanna Dorio, Manuela Porru, Susanna Dolci, Federica Campolo, Patrizia Vernole, Pedro Miguel Lacal, Françoise Praz, Grazia Graziani","doi":"10.3892/ijo.2026.5868","DOIUrl":"10.3892/ijo.2026.5868","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the attention of the Editorial Office that the immunofluorescence images shown in Fig. 3B on p. 214 to represent the 'HCT116 SiP' and 'HCT116+3 SiP' experiments (top row of data) were strikingly similar. Upon examining their data, the authors have realized that the data in Fig. 3B were presented incorrectly; specifically, the data shown in the 'HCT116+3 SiP' panel were erroneously duplicated from the data shown correctly in the 'HCT116 SiP' panel. The authors have now submitted a revised version of Fig. 3, containing the corrected version of the 'HCT116+3 SiP' data panel in Fig. 3B, and this is shown on the next page. Note that this error did not affect the overall conclusions reported in the study. The authors are grateful to the Editor of <i>International Journal of Oncology</i> for allowing them this opportunity to publish a Corrigendum, and all the authors agree with its publication. Furthermore, the authors apologize to the readership for any inconvenience caused. [International Journal of Oncology 43: 210‑218, 2013; DOI: 10.3892/ijo.2013.1932].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13004440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147443723","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":"Crosstalk between KRAS and miRNAs in pancreatic cancer: Opportunities for its diagnosis, prognosis and therapeutic intervention (Review).","authors":"Abdulaziz A Aloliqi, Abdullah M Alnuqaydan, Mohammad Alshebremi, Arshad Husain Rahmani, Amjad Ali Khan","doi":"10.3892/ijo.2026.5873","DOIUrl":"10.3892/ijo.2026.5873","url":null,"abstract":"<p><p>Pancreatic cancer, predominantly manifested as pancreatic ductal adenocarcinoma (PDAC), is a highly aggressive malignancy in which the dysregulated crosstalk between Kirsten rat sarcoma viral oncogene homolog (KRAS) and microRNAs (miRNAs) plays a critical role. It is one of the leading causes of cancer‑related mortality worldwide, with its global incidence more than doubling over the past 25 years. PDAC is characterized by rapid progression, invasiveness and profound resistance to conventional therapies, resulting in dismal prognosis. Its genetic profile is characterized by activating KRAS mutations, present in ~90% of cases. These mutations act as molecular switches that activate multiple intracellular signaling cascades and transcription factors, promoting uncontrolled proliferation, survival, migration and transformation. In addition to direct KRAS alterations, dysregulation of KRAS‑targeting miRNAs further amplify aberrant RAS signaling. Emerging evidences highlights the significant role of miRNAs in driving tumor initiation, progression and metastasis. Several tumor‑suppressive miRNAs that regulate KRAS signaling have demonstrated the capacity to suppress pancreatic tumor development <i>in vitro</i> and in preclinical models. Despite these advances, miRNA‑based therapies, including mimics or anti‑miRNA oligonucleotides targeting KRAS, remain largely unexplored in patients with PDAC. Further, circulating miRNAs show promise as non‑invasive biomarkers for disease detection, monitoring progression and assessment of tumor aggressiveness. The present review provided a concise overview of KRAS signaling and its frequent mutations in PDAC, examines strategies to target KRAS and discussed the crosstalk between KRAS and tumor‑suppressive miRNAs in regulating pancreatic tumorigenesis. It further explored diagnostic and prognostic miRNAs in pancreatic cancer. Collectively, these insights underscored the potential of miRNA‑based interventions to improve early detection, prognosis and targeted therapy in this lethal disease.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13038340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147485936","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":"Selective antitumor and apoptosis‑inducing effects of the Src inhibitor PP1 in human tongue squamous cell carcinoma cells.","authors":"Shirinbaeva Luiza Kantibekovna, Saini Wang, Hyunju Kang, Young-Min Shin, Byeong-Churl Jang","doi":"10.3892/ijo.2026.5877","DOIUrl":"10.3892/ijo.2026.5877","url":null,"abstract":"<p><p>Src phosphorylation (activation) is associated with the proliferation and survival of numerous human cancer cells. The role of Src phosphorylation and expression, as well as its pharmacological inhibition by PP1, a Src inhibitor, in the growth of oral squamous cell carcinoma (OSCC), remain unclear. The present study explored whether Src is expressed and phosphorylated in HSC‑3 human oral cancer cells and whether PP1 treatment affects the proliferation of these cells. Src was found to be highly expressed and phosphorylated in HSC‑3 human oral cancer cells. Notably, treatment with PP1 at 10 µM significantly reduced cell proliferation and induced apoptosis, evidenced by DNA fragmentation, caspase‑9 and ‑8 activation, and poly(ADP‑ribose) polymerase cleavage. Mechanistically, PP1 not only inhibited Src phosphorylation but also disrupted a broad network of oncogenic pathways, including EGFR, JAK2, STAT‑3, PKB and ERK‑1/2 in HSC‑3 cells. Furthermore, PP1 induced markers of ER stress and inhibited protein translation, as shown by increased eIF‑2α phosphorylation and decreased S6 phosphorylation. The critical role of Src was confirmed by pharmacological inhibition and further validated when small interfering RNA‑mediated knockdown mimicked the anti‑proliferative effects of PP1. Importantly, these potent anticancer effects were conserved in another OSCC cell line (YD‑10B) and, were validated in vivo, where PP1 suppressed tumor growth in a zebrafish xenograft model. Collectively, these findings suggest that PP1 exerts strong anticancer effects on human oral cancer by simultaneously inhibiting Src activity and disrupting a network of associated oncogenic pathways (EGFR, STAT‑3, PKB and ERK‑1/2).</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147529127","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":"Multifaceted roles of miR‑124 in cancer: Molecular mechanisms and clinical prospects (Review).","authors":"Jun Guo, Yunyan Guo, Peiyang Chen, Wenyan Xiao, Yuxiang Tan, Zhiyong Wang, Yanxin Lu, Xupeng Yue","doi":"10.3892/ijo.2026.5876","DOIUrl":"10.3892/ijo.2026.5876","url":null,"abstract":"<p><p>MicroRNAs (miRNAs or miRs) are a class of small non‑coding RNAs that are critical regulators of gene expression. By targeting messenger RNAs, they play essential roles in various biological processes, including development, differentiation, immunity, metabolism and apoptosis. miRNA dysregulation is often associated with tumorigenesis and cancer progression. miR‑124, a miRNA predominantly and specifically expressed in the central nervous system, is commonly downregulated in various cancers. It inhibits multiple malignant traits, including tumor growth, metastasis, stemness and chemoresistance. Furthermore, miR‑124 influences the tumor microenvironment and modulates antitumor immune responses. These diverse functions highlight their significant potential for clinical application. Its expression is modulated by various upstream factors, including transcription factors, signaling pathways, epigenetic modifications, and other non‑coding RNAs. However, the precise mechanisms governing this upstream regulation require further investigation. Despite this, the translational application of miR‑124 for early cancer diagnosis and therapy faces several significant challenges, including improving its stability and bioavailability and developing effective <i>in vivo</i> delivery systems. The present study provides a comprehensive overview of the multifaceted roles of miR‑124 in cancer, elucidating its underlying molecular mechanisms and exploring its clinical potential. By synthesizing the current literature, it was aimed to consolidate the current understanding of miR‑124 and identify promising avenues for future research.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13038338/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147529156","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] Knockdown of MALAT1 inhibits osteosarcoma progression via regulating the miR‑34a/cyclin D1 axis.","authors":"Guangchao Duan, Chuanlin Zhang, Changke Xu, Chao Xu, Lei Zhang, Yan Zhang","doi":"10.3892/ijo.2026.5862","DOIUrl":"10.3892/ijo.2026.5862","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the β‑actin control bands shown in Fig. 6D on p. 25 had already been submitted for publication to a different journal in an article written by different authors at different research institutes. In addition, it was also identified that invasion assay data in Fig. 4D and western blot data in Fig. 5E also subsequently appeared in articles in other journals that were written by different authors at different research institutes. Given that the abovementioned contentious data in Fig. 6D had already been submitted for publication elsewhere prior to the submission of this paper 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 54: 17‑28, 2019; DOI: 10.3892/ijo.2018.4600].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12987555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365152","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":"RNA‑binding protein DAZAP1 promotes gastric cancer metastasis by enhancing NOTCH1 and JAG1 mRNA stability.","authors":"Siyang Peng, Yidong Chen, Jieke Wu, Xiaodong Huang, Linjie Hong, Yanci Xie, Yuting Lei, Xiangyang Wei, Ping Yang, Jieming Zhang, Qiong Yang, Guangnan Liu, Aimin Li, Side Liu, Jiaying Li, Weiyu Dai, Yanfeng Hu, Jing Wang, Jing Xiong, Jide Wang","doi":"10.3892/ijo.2026.5863","DOIUrl":"10.3892/ijo.2026.5863","url":null,"abstract":"<p><p>DAZ‑associated protein 1 (DAZAP1), an RNA‑binding protein and modulator of alternative splicing, participates in tumorigenesis. However, the potential oncogenic function and mechanism of DAZAP1 in gastric cancer (GC) are unknown. Gene expression analysis, including mRNA and protein level assessment by reverse transcription‑quantitative PCR and western blotting, respectively, immunofluorescence, immunohistochemistry, <i>in situ</i> hybridization assays, tissue microarray, RNA immunoprecipitation and sequencing and mRNA stability assay were performed, as well as colony formation, EdU, wound healing, migration and invasion assays of GC cells. DAZAP1 displayed a significant upregulation in GC cells and served as an oncogene, as demonstrated by its overexpression promoting colony formation, EdU incorporation, wound healing, migration and invasion, and its knockdown suppressing these malignant phenotypes. Additionally, DAZAP1 upregulation was positively correlated with tumor progression and poor survival in individuals with GC. Functionally, DAZAP overexpression promoted proliferation, epithelial‑mesenchymal transition (EMT) and migration/invasion of GC cells. Mechanistically, DAZAP1 physically bound NOTCH1 or JAG1 mRNA to regulate its stability. In addition, overexpression of DAZAP1 facilitated NOTCH1‑ and/or JAG1‑mediated migration via EMT in GC cells. Changes in NOTCH1 or JAG1 expression were positively correlated with DAZAP1 expression when DAZAP1 was silenced or enhanced in GC. Finally, DAZAP1 modulated the activation of the NOTCH/JAG1 signaling pathway. DAZAP1 expression facilitated migration/invasion and mediated the stabilization of NOTCH1 or JAG1 mRNA, suggesting they may participate in GC progression.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12987562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365179","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] Design, synthesis and preclinical evaluation of NRC‑AN‑019.","authors":"Kompella Amala, A K S Bhujanga Rao, Bharathi Gorantla, Christopher S Gondi, Jasti S Rao","doi":"10.3892/ijo.2026.5866","DOIUrl":"10.3892/ijo.2026.5866","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 images of the experimental mice shown in Figs. 4A and 5A, several sets of mice were positioned in unexpectedly similar orientations, even though details of the luciferase imaging differed a little comparing between the affected data sets. Owing to the number of 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 42: 168‑178, 2013; DOI: 10.3892/ijo.2012.1697].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"68 5","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12987550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365118","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}