Oncology reports最新文献

{"title":"Overcoming melanoma drug resistance: Mechanisms and clinical progress of oncolytic viruses combined with immune checkpoint inhibitors (Review).","authors":"Yuan He, Wenxuan Lin, Haofang Chen, Yongqi Guan, Congcong Guan, Yanxiang Zhang, Dongsheng Pan","doi":"10.3892/or.2026.9197","DOIUrl":"10.3892/or.2026.9197","url":null,"abstract":"<p><p>Although immune checkpoint inhibitors (ICIs) have revolutionized the management of advanced melanoma, a major clinical challenge persists: Nearly 50% of patients develop primary or acquired resistance and therefore derive no meaningful clinical benefit. As ICIs are increasingly used in earlier disease settings, including adjuvant and neoadjuvant therapy, the population of patients with ICI‑resistant disease continues to grow. For patients whose disease progresses after first‑line combined programmed cell death 1 (PD‑1) and cytotoxic T‑lymphocyte associated protein 4 (CTLA‑4) blockade, effective salvage options remain limited, highlighting an urgent unmet medical need. Oncolytic viruses (OVs), which exert antitumor effects through the dual mechanisms of selective tumor cell lysis and immunomodulatory remodeling of the tumor microenvironment, represent a compelling therapeutic strategy for overcoming ICI resistance. Recent clinical and preclinical advances have moved OV‑ICI combination regimens from conceptual strategies to clinically evaluable interventions for refractory melanoma. Nevertheless, several translational barriers impede their broader implementation, including interpatient heterogeneity in treatment response, uncertainty regarding the optimal sequencing and dosing of combination therapies, and the lack of validated predictive biomarkers. The present review systematically synthesizes emerging clinical evidence and mechanistic insights into OV‑ICI synergy to inform rational trial design, refine combination strategies, and accelerate the development of precision immuno‑oncology approaches.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 5","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613317/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990874","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":"Validation of next‑generation sequencing‑derived circulating mRNA variants as potential diagnostic tools in hepatocellular carcinoma and cholangiocarcinoma.","authors":"Daniel Zezulinski, Maarouf A Hoteit, David E Kaplan, Tingting Zhan, Cataldo Doria, Timothy M Block, Aejaz Sayeed","doi":"10.3892/or.2026.9196","DOIUrl":"10.3892/or.2026.9196","url":null,"abstract":"<p><p>Liquid biopsy can transform oncology practice through early detection and real‑time monitoring of cancer progression and response to treatment. Circulating cell‑free tumor RNA offers promise as a novel and emerging alternative to circulating cell‑free tumor DNA for detecting the presence and understanding the biology of liver tumors. Both circulating DNA and RNA, which predominantly reside in extracellular vesicles, carry evidence of vital germline and somatic mutations. High impact single nucleotide changes, insertions and deletions in circulating RNA (ctRNA) serve a key role in cancer development and progression. Tumor cells exploit the RNA splicing machinery to induce structural and functional changes in RNA not transcribed from DNA, thereby promoting tumor growth. Examination of the landscape of mutations in ctRNA using RNA‑sequencing in patients with hepatocellular carcinoma (HCC), cholangiocarcinoma and liver cirrhosis has revealed widespread single nucleotide changes and splicing aberrations associated with patients with cancer. The present study aimed to characterize these next‑generation sequencing‑derived high‑risk circulating mutated RNA (ctmutRNA) variants, and to develop TaqMan chemistry‑based assays for validation of ctmutRNAs in tumor tissues and plasma samples from patients with HCC. The present study identified a short ctmutRNA panel able to distinguish all patients with liver cancer in the discovery cohort, and splicing aberrations, including intron retentions, in tumor tissues were validated. Finally, the present study demonstrated that the assays detecting ctmutRNA analytes in the plasma, if confirmed in larger patient cohorts, could be effectively used to identify patients with HCC. Furthermore, the outstanding questions and challenges that need to be addressed for the development of a robust blood‑based HCC surveillance test are discussed.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 5","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148991017","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] RIP kinase‑mediated ROS production triggers XAF1 expression through activation of TAp73 in casticin‑treated bladder cancer cells.","authors":"Yoon Hee Chung, Daejin Kim","doi":"10.3892/or.2026.9192","DOIUrl":"10.3892/or.2026.9192","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 JNK western blotting data shown in Fig. 2E on p. 1138 were strikingly similar to the JNK western blotting data shown in Fig. 4D on p. 1139, even though the experimental conditions reported for these figure parts were apparently different. The authors have been contacted by the Editorial Office to offer an explanation for the apparent re‑use of the same data in this paper, and the authors have replied to explain that these studies were performed several years ago, that they no longer have access to the original data, and moreover, that they are not in a position to repeat any of these experiments. 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 associated with the abovementioned data. [Oncology Reports 36: 1135‑1142, 2016; DOI: 10.3892/or.2016.4895].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 5","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990916","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] High expression of hnRNPA1 promotes cell invasion by inducing EMT in gastric cancer.","authors":"Yahua Chen, Jun Liu, Wei Wang, Li Xiang, Jide Wang, Side Liu, Hongyan Zhou, Zheng Guo","doi":"10.3892/or.2026.9198","DOIUrl":"10.3892/or.2026.9198","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, an interested reader drew to the Editor's attention that the control GAPDH western blots shown in Fig. 1D on p. 1696 were strikingly similar to the GAPDH blots shown in Fig. 2A on p. 1697, even though the experimental conditions were reported to be different for these figures. In addition, upon analyzing the data in this paper independently in the Editorial Office, it came to light that certain of the hnRNPA1 blots shown in Fig. 1B were strikingly similar to blots that had already been published in a paper in the journal <i>Oncotarget</i> that featured two of the authors in common (Jide Wang and Side Liu). The authors were able to consult their original data, and realized that these data had inadvertently been included incorrectly in these two figures. Revised and corrected versions of Figs. 1 and 2, now showing replacement data for the western blots featured in Figs. 1B, 1D and 2A, are shown on the next two pages. Note that the replacement of the original data with the revised data in this pair of figures has not had a significant impact on the conclusions reached in this study. The authors regret the errors that were made during the compilation of the original figures, and are grateful to the editor of <i>Oncology Reports</i> for allowing them the opportunity to publish this corrigendum. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the readership for any inconvenience caused. [Oncology Reports 39: 1693‑1701, 2018; DOI: 10.3892/or.2018.6273].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 5","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149040240","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] TGF‑β1 mediates epithelial to mesenchymal transition via the TGF‑β/Smad pathway in squamous cell carcinoma of the head and neck.","authors":"Changyun Yu, Yong Liu, Donghai Huang, Yaozhang Dai, Gengming Cai, Jinjie Sun, Ting Xu, Yongquan Tian, Xin Zhang","doi":"10.3892/or.2026.9189","DOIUrl":"10.3892/or.2026.9189","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 Transwell assay data shown in Fig. 2C and 4D, two pairs of overlapping sections of data were identified comparing the panels in these figures, where the results from differently performed experiments were intended to have been portrayed. An Expression of Concern statement was published to account for these concerns (doi: 10.3892/or.2025.9001), after which the authors have responded to the Editorial Office to offer an explanation for this apparent duplication of data within the two figures. To address the issue of the scientific rigor and integrity of this paper, the affected experiments in Figs. 2C and 4D have been performed again in triplicate by the authors. The results obtained were broadly similar to those obtained in the original experiments, and the revised versions of Figs. 2 and 4 are shown on the next page. Also note that the following changes are required to the text in the paper describing the results of these experiments: In the Results section, the corrected data values and text for these experiments should now read as follows: For Fig. 2: 'The cells that invaded through the pores to the lower surface of the filter were <b>29±16</b> and <b>95±36</b> (P<0.05), respectively (Fig. 2C and D)'; and for Fig. 4: 'Smad2 RNAi abrogated the TGF‑β1‑induced suppression of E‑cadherin expression (Fig. 4C) and suppressed the invasion capacity of Tu686 cells (P<0.05, <b>70±22</b> vs. <b>23±8</b>; Fig. 4D and E)'. The data values have also been amended in the respective figure legends for Figs. 2 and 4, as shown on the next page. Note that these errors did not have a significant impact on the conclusions reached in this study. The authors regret the errors that were made during the compilation of the original figures, and are grateful to the editor of <i>Oncology Reports</i> for allowing them the opportunity to publish this Corrigendum. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the readership for any incon-venience caused. [Oncology Reports 25: 1581‑1587, 2011; DOI: 10.3892/or.2011.1251].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 5","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13554944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892172","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":"PINK1 promotes the progression of lung squamous cell carcinoma through the FAK/AKT/RhoA/vinculin pathway.","authors":"Xu Li, Yuhui Ma","doi":"10.3892/or.2026.9201","DOIUrl":"10.3892/or.2026.9201","url":null,"abstract":"<p><p>Lung squamous cell carcinoma (LUSC) is an aggressive malignancy with a poor prognosis. Given the association between mitochondrial dysregulation and LUSC, the aim of the present study was to identify mitochondrial unfolded protein response (UPR^mt)‑related candidate genes associated with LUSC and to explore their potential functional relevance. In the present study, differential expression, univariate Cox and survival analyses were combined to identify a UPR^mt‑associated key gene in LUSC. Gene set enrichment analysis was then performed, and overexpression (OE) and knockdown cell lines were used to clarify its function using western blotting, Cell Counting Kit‑8, colony formation and Transwell^® invasion assays. Using bioinformatics tools and a review of the literature, PTEN‑induced kinase 1 (PINK1) was singled out as a key gene in LUSC samples. Elevated PINK1 expression was associated with worse survival outcomes. A total of 117 pathways were enriched by PINK1, with the top 5 including 'focal adhesion' and 'mitogen‑activated protein kinase signaling pathway'. Using experimental analysis, it was observed that PINK1 significantly enhanced the proliferative, migratory, invasive and colony forming abilities of tumor cells, thereby exacerbating LUSC. Furthermore, these enhancements were diminished by the application of focal adhesion kinase (FAK) inhibitor. It was also noted that the expression levels of protein kinase B (AKT), p‑AKT, Ras homolog family member A (RhoA) and vinculin were all elevated in OE‑PINK1 cells. Collectively, these findings indicated that PINK1 exerted its influence on LUSC through the FAK/AKT/RhoA/vinculin pathway. The present study identified PINK1 as a key gene in LUSC, exerting its influence through the FAK/AKT/RhoA/vinculin pathway, thereby presenting a potential novel therapeutic target for the treatment of LUSC in the future.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 5","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13646776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112754","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":"Loperamide enhances the radiosensitivity of cervical cancer cells via ferroptosis induction.","authors":"Huarong Guo, Haixia Li, Shunkang Tian, Yunkai Zhang, Fuyun Wu, Jing Ke","doi":"10.3892/or.2026.9203","DOIUrl":"10.3892/or.2026.9203","url":null,"abstract":"<p><p>Cervical cancer is a malignant tumor that threatens women's health and radiotherapy represents a major therapeutic approach for its treatment; however, radioresistance frequently leads to treatment failure. The present study aimed to investigate whether loperamide (LOP), a µ‑opioid receptor agonist commonly used as an antidiarrheal agent, could enhance the radiosensitivity of cervical cancer cells by regulating ferroptosis. A Cell Counting Kit‑8 assay was used to evaluate the cytotoxicity of LOP in SiHa and HeLa cells, and EdU and colony formation assays were performed to assess cell proliferation. In addition, wound‑healing and Transwell assays were performed to detect cell migration. Flow cytometry was applied to measure cell apoptosis and intracellular reactive oxygen species (ROS) levels, and colorimetric assays were used to determine malondialdehyde (MDA) and glutathione (GSH) contents. The mRNA and protein expression levels of the ferroptosis‑related markers GSH peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) were analyzed using reverse transcription‑quantitative PCR and western blotting. The results showed that LOP significantly inhibited the viability of SiHa and HeLa cells, and exerted a synergistic effect with radiotherapy (combination index <1) to suppress cell proliferation and migration. Combined treatment with LOP and radiotherapy markedly increased apoptosis and ROS accumulation, elevated MDA levels and reduced GSH levels. Moreover, the combination treatment significantly downregulated the expression of GPX4 and SLC7A11. These findings indicated that LOP enhances the radiosensitivity of cervical cancer cells, with ferroptosis induction via inhibition of the GPX4/SLC7A11 axis as a contributing mechanism. Both apoptosis and ferroptosis were induced by the combination treatment, suggesting that the radiosensitizing effect may involve multiple cell death pathways. These observations provide a basis for further investigation into LOP as a potential radiosensitizing agent in cervical cancer.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 5","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13646775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112781","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] The interaction between miR‑148a and DNMT1 suppresses cell migration and invasion by reactivating tumor suppressor genes in pancreatic cancer.","authors":"Le Hong, Gen Sun, Long Peng, Yi Tu, Zhen Wan, Haiwei Xiong, Yong Li, Weidong Xiao","doi":"10.3892/or.2026.9195","DOIUrl":"10.3892/or.2026.9195","url":null,"abstract":"<p><p>Subsequently to the publication of the above article, an interested reader drew to the Editor's attention that, in Fig. 2C and D on p. 2921 showing the methylation status of the miR‑148a promoter, the centrally placed 'M' and 'U' lanes in these figure parts apparently showed the same data, albeit with horizonal stretching of the bands in question. Furthermore, in Fig. 6B on p. 2923, which showed the results of cell migration and invasion assay experiments, the 'Mimics‑NC/Migration' and 'Blank/Invasion' data panels apparently showed the same data, albeit with different sizing of the panels, such that these were derived from the same orginal source. Finally, the reader noted that one of the antibodies the authors had used in their study was apparently selected inappropriately: The antibody (cat. no. ab51243) that the authors reported to have used is specific for the protein known as p16‑ARC (or ARPC5), not the apoptosis‑associated protein p16‑INK4a, as was intended. The authors were asked to investigate these various matters, and have fully responded to the reader's queries. Concerning the antibody, after thoroughly examining the original reagent purchase records and raw experimental data, the authors can confirm that the correct anti‑CDKN2A/p16 antibody (cat. no.  ab108349; Abcam) was in fact used in this study: As the catalogue number of antibody was not stated in the initial manuscript submission and this information was requested during the editing stage of the paper, the authors inadvertently entered the incorrect catalogue number into the text of the paper (they also provided a copy of the original purchase form to the Editorial Office for our inspection). Therefore, the sentence commencing on p. 2918, left‑hand column, line 20, in the '<i>Protein extraction and western blot analysis</i>' subsection of the Materials and methods section should have read as follows: 'The primary antibodies used were as follows: DNMT1 (1:500, cat. no. ab188453; Abcam), p16 (1:200, cat. no. ab108349; Abcam)...'.Concerning Figs. 2 and 6, the authors were able to examine their original data, and realized that errors had inadvertently been made when assembling these figures. Corrected versions of Figs. 2 and 6, now showing data from one of the repeated sets of experiments for Fig. 2A‑D and the correct data for the 'Blank/Invasion' data panel in Fig. 6B, are shown on the next two pages. The authors wish to emphasize that the errors made in assembling the data in these figures did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of <i>Oncology Reports</i> for granting them this opportunity to publish a Corrigendum, and apologize to both the Editor and the readership for any inconvenience caused; they also thank the reader of the article for drawing these matters to their attention. [Oncology Reports 40: 2916‑2925, 2018; DOI: 10.3892/or.2018.6700].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 5","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990910","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":"Mitochondrial mechanisms underlying spatial immune phenotypes in non‑small cell lung cancer: Implications for ICI response and cold‑to‑hot tumor conversion (Review).","authors":"Hongyi Lai, Ke Sun, Tong Mu, Xi Liu, Mingshan Liu","doi":"10.3892/or.2026.9202","DOIUrl":"10.3892/or.2026.9202","url":null,"abstract":"<p><p>Non‑small cell lung cancer (NSCLC) is characterized by marked spatial immune heterogeneity, commonly manifested as immune‑desert, immune‑excluded and immune‑inflamed phenotypes. These phenotypes are closely associated with variable responses to immune checkpoint inhibitors (ICIs). Emerging evidence suggests that they are shaped not only by canonical immune pathways but also by mitochondrial processes that regulate immune priming, T‑cell trafficking and the maintenance of effector function. The present review summarizes how mitochondrial reactive oxygen species, mitochondrial DNA‑cGAS‑STING signaling, pathways mediated by tricarboxylic acid cycle metabolites, and non‑cell‑autonomous mitochondrial transfer may contribute to the establishment and maintenance of distinct spatial immune phenotypes in NSCLC. It is proposed that insufficient activation of innate immunity and impaired dendritic cell priming are particularly relevant to immune‑desert tumors, whereas chronic oxidative stress may reinforce barriers mediated by cancer‑associated fibroblasts (CAFs), transforming growth factor β, and the extracellular matrix in immune‑excluded tumors. By contrast, immune‑inflamed tumors may represent a state in which pre‑existing immune circuitry remains intact and tumor‑infiltrating lymphocytes retain greater mitochondrial fitness and metabolic resilience. The implications of these mechanisms for ICI sensitivity and cold‑to‑hot tumor conversion strategies were further discussed. Current evidence from human studies remains largely correlative, and prospective, spatially resolved functional studies are needed. Nevertheless, integrating mitochondrial biology with spatial immune architecture within a phenotype‑guided framework may generate testable hypotheses for future biomarker development and combination strategies.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 5","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13646777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112738","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] MicroRNA‑195‑5p is a potential diagnostic and therapeutic target for breast cancer.","authors":"Qifeng Luo, Chuankui Wei, Xiaoyu Li, Jia Li, Lei Chen, Yixiang Huang, Hongming Song, Dengfeng Li, Lin Fang","doi":"10.3892/or.2026.9200","DOIUrl":"10.3892/or.2026.9200","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned author drew to the authors' attention that, regarding the cell migration assay experiments shown in Fig. 4 on p. 1099, Fig. 4B and C, showing the results of the 'NC' and 'Mock' experiments, contained an overlapping section of data, suggesting that these data panels were derived from the same original source where different experiments were intended to have been portrayed.  The authors have been contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of this potential issue concerning 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. [Oncology Reports 31: 1096‑1102, 2014; DOI: 10.3892/or.2014.2971].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 5","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13635724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149040176","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}