Oncol. Rep. [JOURNAL]
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200 papers
[Retracted] MicroRNA‑302a targets GAB2 to suppress cell proliferation, migration and invasion of glioma.
Ma J, Yu J, Liu J … +6 more , Yang X, Lou M, Liu J, Feng F, Ji P, Wang L
Oncol Rep · 2026 Jan · PMID 41170780 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that cell invasion and migration assay data featured in Fig. 5C on p. 1164 were strikingly similar to data that a...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that cell invasion and migration assay data featured in Fig. 5C on p. 1164 were strikingly similar to data that already been submitted for publication to the journal in a paper written by different authors at different research institutes. Moreover, cell invasion and migration assay data panels both within Fig. 6C, and comparing Fig. 6C with Fig. 5C, revealed a number of internally overlapping panels, suggesting that data which were intended to have shown the results from differently performed experiments had apparently been derived from a smaller number of original sources. Owing to the fact that the abovementioned data had already been submitted for publication prior to the receipt of this article at , 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. [Oncology Reports 37: 1159‑1167, 2017; DOI: 10.3892/or.2016.5320].
[Corrigendum] Gemcitabine combined with an engineered oncolytic vaccinia virus exhibits a synergistic suppressive effect on the tumor growth of pancreatic cancer.
Chen W, Fan W, Ru G … +5 more , Huang F, Lu X, Zhang X, Mou X, Wang S
Oncol Rep · 2026 Jan · PMID 41170768 · Full text
Following the publication of the above article, the authors drew to the Editor's attention that certain of the data in Fig. 6 on p. 74 had been assembled incorrectly. Specifically, the data panels showing the results of...
Following the publication of the above article, the authors drew to the Editor's attention that certain of the data in Fig. 6 on p. 74 had been assembled incorrectly. Specifically, the data panels showing the results of the SW1990/oVV/H&E and the SW1990/GEM/oVV/H&E experiments, and the SW1990/Gemcitabine/IHC‑Smac and the SW1990/GEM/oVV/IHC‑Smac experiments, respectively, contained overlapping sections, such that the data, which were intended to show the results of differently performed experiments, had been derived from the same original sources. Furthermore, upon performing an independent analysis of the data in the Editorial Office, it was noted that the data panels selected for the SW1990/oVV‑Smac/TUNEL and the SW1990/Gemcitabine&oVV‑Smac/TUNEL experiments also contained overlapping sections, and concerning the western blot data shown in Fig. 3B on p. 71, the Survivin protein bands were strikingly similar to data which had appeared in an earlier paper featuring some of the same authors in the journal . After having re‑examined these figures, the authors realized that these additional cases of data duplication/re‑use were also in need of correction. The revised versions of Figs. 3 and 6, now showing the correct data for the SW1990/GEM/oVV/H&E, SW1990/GEM/oVV/IHC‑Smac and SW1990/oVV‑Smac/TUNEL experiments in Fig. 3, and the correct Survivin western blot data in Fig. 6, are shown on the next page. The authors wish to emphasize that the errors made in terms of the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of for granting them this opportunity to publish a Corrigendum, and apologize to both the Editor and the readership for any inconvenience caused. [Oncology Reports 41: 67‑76, 2019; DOI: 10.3892/or.2018.6817].
CD44 knockdown and TGF‑β inhibition modulate cell proliferation and invasion in claudin‑low breast cancer cells.
Matsunuma R, Kinoshita K, Imada S … +3 more , Sato S, Hayami R, Tsuneizumi M
Oncol Rep · 2026 Jan · PMID 41170763 · Full text
CD44 serves a dual role in supporting tumor survival and promoting invasion. Claudin‑low breast cancer, characterized by a CD44/CD24 phenotype and epithelial‑mesenchymal transition (EMT), displays aggressive behavior. Th...
CD44 serves a dual role in supporting tumor survival and promoting invasion. Claudin‑low breast cancer, characterized by a CD44/CD24 phenotype and epithelial‑mesenchymal transition (EMT), displays aggressive behavior. The present study investigated the interaction between CD44 and TGF‑β signaling, and assessed the cellular effects of their combined inhibition. CD44 was knocked down in claudin‑low breast cancer cell lines (SUM159 and MDA‑MB‑231), and the TGF‑β receptor (TGFBR) inhibitor LY2109761 (LY‑61) was applied for treatment. Cell viability (MTT assay), apoptosis (annexin V assay), invasion (Transwell assay), colony formation and Smad2 phosphorylation (western blotting) were evaluated. CD44 knockdown reduced viability and increased apoptosis but did not markedly suppress invasion. Although TGF‑β stimulation enhanced Smad2 phosphorylation, CD44 knockdown alone did not increase Smad2 activation, indicating that it does not directly regulate Smad2. However, LY‑61 inhibited TGF‑β‑induced Smad2 phosphorylation, effectively counteracting pro‑invasive signaling. Notably, while CD44 knockdown alone had a negligible impact on invasion, its combination with LY‑61 markedly reduced the invasive capacity and colony formation of cells compared with the control (control cells transduced with non‑targeting short hairpin RNA without LY‑61 treatment). LY‑61 induced S phase accumulation, which was more pronounced in SUM159 cells than in MDA‑MB‑231 cells, indicating cell line‑specific effects on cell‑cycle regulation. Clinical data indicated that low CD44 expression was associated with improved survival in patients with claudin‑low breast cancer, despite its potential to enhance EMT signaling. These findings suggested that CD44 knockdown enhanced the response to TGFBR inhibition. Although CD44 depletion may increase EMT‑related signaling, invasion was primarily suppressed by TGF‑β blockade, and the combination with CD44 knockdown further enhanced the inhibition of proliferative phenotypes compared with either treatment alone. This dual‑targeting approach warrants further investigation in claudin‑low breast cancer.
Comparative analysis of the efficacy and safety of antibody‑drug conjugates, radionuclide‑drug conjugates and their combination targeting claudin 18.2 in gastric cancer treatment.
Du H, Hao XF, Lin BW … +11 more , Zhang Y, Rui L, Wang J, Tang MM, Wang DC, Zhu YH, Li J, Dai TZ, Yang Y, Yang X, Du X
Oncol Rep · 2026 Jan · PMID 41133465 · Full text
Gastric cancer (GC) is one of the most common types of cancer worldwide, with limited therapeutic options available for patients with advanced‑stage disease. Claudin 18.2 (CLDN18.2) has emerged as a popular target for th...
Gastric cancer (GC) is one of the most common types of cancer worldwide, with limited therapeutic options available for patients with advanced‑stage disease. Claudin 18.2 (CLDN18.2) has emerged as a popular target for the diagnosis and treatment of GC. Although antibody‑drug conjugates (ADCs) and radionuclide‑drug conjugates (RDCs) targeting CLDN18.2 have been assessed, to the best of our knowledge, no comparative studies have evaluated the efficacy and toxicity profiles of these two treatment modalities. The present study aimed to compare the antitumor efficacy and toxicity of ADCs and RDCs derived from the same anti‑CLDN18.2 monoclonal antibody (mAb) targeting CLDN18.2‑positive tumors. Modified DFO/DOTA‑SYSA1801mAb, labeled with Zr and Lu, was used in cell‑based assays, positron emission tomography and biodistribution studies to evaluate its targeting specificity. In an NUGC‑4‑CLDN18.2 xenograft tumor model, the antitumor efficacy and toxicity of the mAb (SYSA1801mAb), as well as the ADC (SYSA1801) and RDC ([Lu]Lu‑DOTA‑SYSA1801mAb), and their combinations in different sequences (ADC→RDC and RDC→ADC), were systematically assessed. [Zr]Zr‑DFO‑SYSA1801mAb demonstrated notable stability and effectively imaged tumors with high CLDN18.2 expression. [Lu]Lu‑DOTA‑SYSA1801mAb exhibited strong tumor‑targeting ability, with significantly higher tumor uptake than other tissues. By day 145, the complete remission (CR) rate in the ADC group was 60%, with an overall survival (OS) rate of 60%. In the ADC→RDC group, the CR and OS rates were both 40%. The OS rates in the RDC, RDC→ADC, mAb and control groups were all 0%. The ADC group exhibited minimal changes in hematological parameters and hepatic/renal function, whereas the RDC and RDC→ADC groups showed more significant changes. These preclinical findings suggested that ADC monotherapy may demonstrate superior efficacy and safety profiles when compared with RDC monotherapy. Furthermore, sequential combination therapy that starts with ADC appears to be more favorable than approaches that start with RDC. Although ADC→RDC sequential therapy did not significantly outperform ADC monotherapy in this model, it may serve as an effective subsequent treatment strategy.
LRRC59 inhibits perk pathway‑induced apoptosis and promotes cell proliferation, migration and invasion in colorectal cancer cells.
Hou X, Wang Y, Chen Y … +6 more , Zhong P, Wang G, Li B, Lu B, Jiang H, Ning S
Oncol Rep · 2026 Jan · PMID 41133451 · Full text
Leucine‑rich repeat‑containing protein 59 (LRRC59), a 244‑amino‑acid endoplasmic reticulum membrane protein, is implicated in the tumorigenesis of multiple malignancies. However, its functional significance in colorectal...
Leucine‑rich repeat‑containing protein 59 (LRRC59), a 244‑amino‑acid endoplasmic reticulum membrane protein, is implicated in the tumorigenesis of multiple malignancies. However, its functional significance in colorectal cancer (CRC) remains poorly understood. In the present study, LRRC59 expression in CRC tissues was evaluated using immunohistochemistry and western blotting. Colony formation, Cell Counting Kit‑8, wound healing and Transwell assays, in xenograft models, were used to evaluate the effect of LRRC59 on CRC progression. Apoptosis was analyzed using flow cytometry and western blotting. The interaction between LRRC59 and the protein kinase RNA‑like endoplasmic reticulum kinase (PERK) pathway was verified using the starBase database and western blotting. It was found that LRRC59 expression was significantly higher in CRC tissues than in normal tissues. LRRC59 knockdown in HCT116 and LoVo cells inhibited proliferation, migration and invasion and promoted apoptosis, and the PERK pathway was significantly activated. subcutaneous tumorigenesis assays corroborated these findings. Treatment with a PERK pathway‑specific inhibitor reduced the apoptosis of HCT116 and LoVo cells with LRRC59 knockdown. These findings suggest that LRRC59 is not only significantly upregulated in CRC but also mechanistically drives tumor progression by coordinating pro‑oncogenic processes, including enhanced proliferation, migration and invasion. Importantly, mechanistic evidence was provided that LRRC59 inhibits apoptosis by suppressing the PERK signaling axis, identifying this molecule a target in the development of CRC therapeutic strategies.
Targeting cell death pathways in acute myeloid leukemia: Molecular mechanisms and clinical implications (Review).
Jianati R, Chen H, Yang X … +6 more , Yan L, Guo Y, Fan C, Hao X, Zhu G, Shi Z
Oncol Rep · 2025 Dec · PMID 41104889 · Full text
Acute myeloid leukemia (AML) is a highly heterogeneous hematologic malignancy, characterized by complex molecular features and mechanisms of treatment resistance, which lead to a poor prognosis and high relapse rates. Th...
Acute myeloid leukemia (AML) is a highly heterogeneous hematologic malignancy, characterized by complex molecular features and mechanisms of treatment resistance, which lead to a poor prognosis and high relapse rates. The complexity of multi‑pathway interactions and the dysregulated dynamics of tumor cell death pathways may contribute to the wide range of clinical outcomes observed despite advancements in current therapies. Most current research focuses on a single form of cell death, neglecting the mechanisms of other death pathways and their synergistic interactions, which hinders the development of novel therapeutic approaches. The present review systematically integrates and compares the molecular features of key cell death modalities in AML, including autophagy, apoptosis, pyroptosis, necroptosis, ferroptosis and cuproptosis. The present review analyzes their specific triggers, signaling hubs and regulatory networks within the metabolic microenvironment, and discusses the dynamic crosstalk among these pathways. A key focus is the therapeutic potential of exploiting this crosstalk to design synergistic combination therapies. To overcome the limitations of conventional treatments and improve patient outcomes, it is essential to further investigate the transition mechanisms of various cell death modes in AML progression, drug resistance and relapse. Additionally, establishing a theoretical foundation for the development of innovative therapies that synergistically regulate multiple death pathways is crucial.
[Expression of Concern] CDKN3 is an independent prognostic factor and promotes ovarian carcinoma cell proliferation in ovarian cancer.
Li T, Xue H, Guo Y … +1 more , Guo K
Oncol Rep · 2026 Jan · PMID 41104877 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the cell invasion assay data shown in the three panels of Fig. 6A appeared to contain overlapping sections at dif...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the cell invasion assay data shown in the three panels of Fig. 6A appeared to contain overlapping sections at different orientations (all three panels), even though the data were apparently meant to show the results of experiments performed under different conditions. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper; however, 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 continues to investigate this matter further. [Oncology Reports 31: 1825‑1831, 2014; DOI: 10.3892/or.2014.3045].
[Expression of Concern] Knockdown of Bmi1 inhibits the stemness properties and tumorigenicity of human bladder cancer stem cell‑like side population cells.
Zhu D, Wan X, Huang H … +6 more , Chen X, Liang W, Zhao F, Lin T, Han J, Xie W
Oncol Rep · 2026 Jan · PMID 41104865 · Full text
Following the publication of this paper, a concerned reader drew to the Editor's attention that the positioning and proportions of the first and third mice (from the left) in Fig. 7A were very similar, raising a possible...
Following the publication of this paper, a concerned reader drew to the Editor's attention that the positioning and proportions of the first and third mice (from the left) in Fig. 7A were very similar, raising a possible concern that the same mouse had been used to show the experiments in these cases. The authors were contacted by the Editorial Office to offer an explanation for this potential anomaly in the presentation of the data in this paper; however, 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 continues to investigate this matter further. [Oncology Reports 31: 727‑736, 2014; DOI: 10.3892/or.2013.2919].
Platelet‑circulating tumor cell crosstalk: A pivotal target in cancer diagnosis and therapy (Review).
Zhang L, Yuan Y, Deng Y … +2 more , Wang L, Chen F
Oncol Rep · 2026 Jan · PMID 41104864 · Full text
Platelets, while essential for hemostasis, have been recognized as critical mediators in cancer metastasis. The crosstalk between platelets and circulating tumor cells (CTCs) constitutes a key driver of metastasis, emerg...
Platelets, while essential for hemostasis, have been recognized as critical mediators in cancer metastasis. The crosstalk between platelets and circulating tumor cells (CTCs) constitutes a key driver of metastasis, emerging as a focal point in oncology research. Elucidating the underlying mechanisms provides novel insights into tumor dissemination. The present review systematically traces the evolution of platelet‑CTC crosstalk, from receptor‑mediated adhesion to bidirectional molecular exchange, and its implications for metastatic progression. Additionally, the diagnostic significance of platelet‑CTC complexes as potential biomarkers for cancer detection and prognosis is highlighted. Finally, promising therapeutic strategies targeting the platelet‑CTC crosstalk are discussed. By integrating current knowledge, it was demonstrated that targeting platelet‑CTC crosstalk holds potential for improving cancer diagnosis and therapy, while also identifying avenues for future translational research.
[Expression of Concern] Combination of the FGFR4 inhibitor PD173074 and 5‑fluorouracil reduces proliferation and promotes apoptosis in gastric cancer.
Ye YW, Hu S, Shi YQ … +6 more , Zhang XF, Zhou Y, Zhao CL, Wang GJ, Wen JG, Zong H
Oncol Rep · 2025 Dec · PMID 41070624 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the western blot data shown in Figs. 1E and 4, the FGFR blots and control GAPDH blots were both strikingly s...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the western blot data shown in Figs. 1E and 4, the FGFR blots and control GAPDH blots were both strikingly similar in these figures, suggesting that the same data had been included in these, even though the results from differently performed experiments were intended to have been portrayed. The authors were contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in this paper; however, 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 continues to investigate this matter further. [Oncology Reports 30: 2777‑2784, 2013; DOI: 10.3892/or.2013.2796].
m6A reader IGF2BP2 mediates paclitaxel resistance in esophageal squamous cell carcinoma via FOXM1 mRNA stabilization.
Ren S, Wu J, Zhang L … +2 more , Guan G, Jiang W
Oncol Rep · 2025 Dec · PMID 41041871 · Full text
Esophageal squamous cell carcinoma (ESCC) ranks among the primary contributors to cancer‑related mortality in China. Resistance to paclitaxel markedly diminishes its therapeutic effectiveness and outcomes. Anaerobic glyc...
Esophageal squamous cell carcinoma (ESCC) ranks among the primary contributors to cancer‑related mortality in China. Resistance to paclitaxel markedly diminishes its therapeutic effectiveness and outcomes. Anaerobic glycolysis is a pivotal mechanism in cancer progression. Insulin‑like growth factor 2 mRNA binding protein 2 (IGF2BP2) as a reader of RNA N6‑methyladenosine (m6A) modification ensures the stability of RNA at the post‑transcriptional level. Nonetheless, the role and mechanism of IGF2BP2 in mediating paclitaxel resistance and anaerobic glycolysis in ESCC remain unclear. The current study selected two ESCC cell lines (KYSE30 and KYSE150). Cell proliferation and clonogenic ability were assessed via functional experiments. Apoptosis was quantified through flow cytometry. The rate of anaerobic glycolysis was determined via glycolysis assays. The stability of Forkhead box M1 (FOXM1) mRNA was assessed through reverse transcription‑quantitative polymerase chain reaction following actinomycin D treatment. Protein levels were analyzed through western blotting. Bioinformatics analysis revealed an overexpression of IGF2BP2 in ESCC. Furthermore, IGF2BP2 silencing inhibited cell proliferation and clonogenic activity. RNA and m6A‑sequencing results suggested that FOXM1 is critical to IGF2BP2‑mediated paclitaxel resistance in ESCC. Additionally, it was discovered that the silencing of IGF2BP2 compromises FOXM1 mRNA stability, reduces anaerobic glycolysis, and diminishes paclitaxel resistance. Finally, FOXM1 overexpression mitigated the effects of IGF2BP2 silencing in ESCC cells. The current findings underscore the significant role of the IGF2BP2‑FOXM1 signaling pathway in modulating anaerobic glycolysis and paclitaxel resistance in ESCC, offering insights into future therapeutic approaches to this malignancy.
Molecular mechanisms and potential targeting strategies of ubiquitin‑proteasome system‑mediated PD‑1/PD‑L1 ubiquitination in tumor immune suppression (Review).
Gu LH, Guo A, Ding YY … +4 more , Wang XJ, Zhang HX, Duan WL, Zhang BG
Oncol Rep · 2025 Dec · PMID 41041864 · Full text
Cancer cells play a pivotal role in immune evasion by activating the programmed cell death protein 1 (PD‑1)/PD‑ligand (L)1 signaling pathway or immune cells within the tumor microenvironment. The ubiquitin‑proteasome sys...
Cancer cells play a pivotal role in immune evasion by activating the programmed cell death protein 1 (PD‑1)/PD‑ligand (L)1 signaling pathway or immune cells within the tumor microenvironment. The ubiquitin‑proteasome system (UPS), the primary pathway for intracellular protein degradation, has been increasingly implicated in mediating tumor immune escape and resistance to anti‑PD‑1/PD‑L1 therapy. Targeting the UPS has demonstrated significant potential in improving the efficacy of tumor immunotherapy. Therefore, a deeper understanding of the molecular mechanisms by which UPS contributes to tumor resistance against PD‑1/PD‑L1 blockade, along with the optimization of UPS‑targeted small‑molecule drug design, holds scientific and clinical significance. In the present review, the role of UPS in tumor immune evasion through the regulation of PD‑1/PD‑L1 ubiquitination was discussed and potential therapeutic agents that may enhance the effectiveness of anti‑PD‑1/PD‑L1 treatment are summarized. These insights provide a theoretical foundation for advancing cancer immunotherapy and developing novel combination strategies.
miR‑100‑5p and miR‑203a‑3p suppress esophageal squamous cell carcinoma progression by targeting FKBP5.
Tanaka H, Maruyama S, Shoda K … +12 more , Kawaguchi Y, Higuchi Y, Ozawa T, Nakayama T, Saito R, Izumo W, Takiguchi K, Shiraishi K, Furuya S, Amemiya H, Kawaida H, Ichikawa D
Oncol Rep · 2025 Dec · PMID 41041863 · Full text
Poorly differentiated cancers, including esophageal squamous cell carcinoma (ESCC), exhibit higher malignant potential and worse prognoses than well‑differentiated types. The present study aimed to identify microRNAs (mi...
Poorly differentiated cancers, including esophageal squamous cell carcinoma (ESCC), exhibit higher malignant potential and worse prognoses than well‑differentiated types. The present study aimed to identify microRNAs (miRNAs or miRs) involved in ESCC progression and their target mRNAs, focusing on tumor differentiation. miRNA candidates were selected using a miRNA array‑based approach and GEO datasets, comparing expression levels between poorly and non‑poorly differentiated ESCC. Clinical samples (n=61) and cell lines were analyzed to determine the significance and function of the selected miRNAs and their target mRNA. miR‑100‑5p and miR‑203a‑3p were significantly downregulated in poorly differentiated ESCC, with lower expression strongly associated with poorer overall survival (OS) (miR‑100‑5p: P=0.02; miR‑203a‑3p: P=0.05) and relapse‑free survival (RFS) (miR‑100‑5p: P=0.04; miR‑203a‑3p: P=0.12). Overexpression of these miRNAs suppressed cell migration and invasion. was identified as a common target, with its expression significantly reduced upon double‑transfection with miR‑100‑5p and miR‑203a‑3p. downregulation reduced tumor aggressiveness in KYSE70 cells, and clinical samples showed significantly worse survival rates in patients with high expression (OS: P=0.02; RFS: P=0.04). These findings suggest that miR‑100‑5p and miR‑203a‑3p act as tumor suppressors by targeting , highlighting as a potential therapeutic target in ESCC.
[Expression of Concern] TGF‑β1 mediates epithelial to mesenchymal transition via the TGF‑β/Smad pathway in squamous cell carcinoma of the head and neck.
Yu C, Liu Y, Huang D … +6 more , Dai Y, Cai G, Sun J, Xu T, Tian Y, Zhang X
Oncol Rep · 2025 Dec · PMID 41041840 · Full text
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...
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. The authors were contacted by the Editorial Office to offer an explanation for this apparent duplication of data within the two figures; however, 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 continues to investigate this matter further. [Oncology Reports 25: 1581‑1587, 2011; DOI: 10.3892/or.2011.1251].
The silent players: Atypical isoforms as biomarkers and therapeutic hurdles in CML pathogenesis (Review).
Zhou X, Li A, Kong D … +3 more , Shi Y, Zhang P, Shan N
Oncol Rep · 2025 Dec · PMID 40999990 · Full text
Chronic myeloid leukemia (CML) is a hematological malignancy driven by diverse genetic aberrations, with the Philadelphia chromosome and its resultant fusion gene constituting key pathogenic drivers. Atypical fusion tra...
Chronic myeloid leukemia (CML) is a hematological malignancy driven by diverse genetic aberrations, with the Philadelphia chromosome and its resultant fusion gene constituting key pathogenic drivers. Atypical fusion transcripts have distinctive structural and functional properties. Structural divergence in these variants leads to functional alterations of encoded oncoproteins, potentially influencing disease progression and therapeutic responsiveness. Conventional diagnostic modalities, including reverse transcription‑PCR and fluorescence in situ hybridization, may fail to detect rare variants, necessitating complementary high‑sensitivity techniques such as next‑generation sequencing). Tyrosine kinase inhibitors (TKIs), including imatinib and dasatinib, remain cornerstone treatments; however, marked inter‑variant heterogeneity in TKI responsiveness is observed: Patients harboring transcripts generally show favorable prognoses, while those with variants demonstrate an increased risk of relapse and/or TKI resistance, often requiring multimodal strategies combining chemotherapy or allogeneic hematopoietic stem cell transplantation. Although Chimeric Antigen Receptor)‑T cell therapy has shown promise in treating (Philadelphia chromosome‑positive B‑cell Acute Lymphoblastic Leukemia, its application in CML, particularly in variants such as or , is not currently recommended as a first‑line treatment. Despite advances in elucidating the clinical implications of fusion gene heterogeneity in leukemogenesis, the prognostic value of atypical isoforms requires further validation through multicenter studies with extended cohorts. This review aimed to summarize cases of atypical fusion genes in CML, with analysis of clinical characteristics, therapeutic interventions, and prognostic outcomes, to provide clinicians with enhanced reference material for improved patient management.
Neuroscience in glioma biology (Review).
Zhang C, Zhang H, Cao J … +1 more , Liu M
Oncol Rep · 2025 Dec · PMID 40999988 · Full text
Although our understanding of the molecular and cellular factors involved in the development and growth of glioma has increased, prognosis remains dismal in most patients. The emerging field of cancer neuroscience has re...
Although our understanding of the molecular and cellular factors involved in the development and growth of glioma has increased, prognosis remains dismal in most patients. The emerging field of cancer neuroscience has revealed the intricate functional interplay between glioma and the cellular architecture of the brain, especially neural circuits. In recent years, studies have revealed that glioma cells integrate and remodel multicellular neural circuits. Neural circuits have thus emerged as critical regulators of glioma from initiation to malignant growth. In the present review, an updated framework was provided for understanding the construction of neuron‑glioma networks and the mechanisms by which neurons regulate the malignant phenotype of glioma. Readers will also obtain insights into the construction of glioma‑glioma networks formed by tumor microtubes. Furthermore, the present review reveals the complex interconnectivity among the nervous system, immune system and glioma that promotes tumor growth. Finally, some potential areas of clinical translation and new research directions were highlighted.
Multiple roles of replication factor C family in pan‑cancer (Review).
Luo D, Li B, Jiang X
Oncol Rep · 2025 Dec · PMID 40999981 · Full text
Due to the persistently high global incidence and mortality rates of cancer, developing novel therapeutic strategies is imperative. The replication factor C (RFC) family, a critical subset of DNA replication and repair,...
Due to the persistently high global incidence and mortality rates of cancer, developing novel therapeutic strategies is imperative. The replication factor C (RFC) family, a critical subset of DNA replication and repair, serves multifaceted roles in tumor progression. Despite its widely recognized importance, the pleiotropic mechanisms of the RFC family lack systematic illustration, particularly regarding each member specific contributions to cancer hallmarks. In the present review, mRNA expression of each RFC family member in pan‑cancer was profiled and the associations between their expression levels and tumor types evaluated. In addition, the effect of RFC expression on patients' survival across malignancies is assessed. Furthermore, the present review summarized current research on RFC family members in various malignancies with particular emphasis on the RFC‑like complexes, highlighting key findings and advancements in understanding their role in tumor biology. The signaling pathways associated with RFC family members are discussed and the molecular mechanisms elucidated. Finally, the clinical importance of RFC family members including prognosis, potential inhibitors and combination treatments are also discussed. The present review aimed to provide innovative perspectives for developing combinatorial molecular targeted therapies in the future.
Relationship between amino acid transporter activity and radioactive iodine therapy efficacy in differentiated thyroid cancer.
Kotani A, Tatara Y, Sakamoto R … +3 more , Wojcik A, Mariya Y, Monzen S
Oncol Rep · 2025 Dec · PMID 40999970 · Full text
Thyroid cancer is the most common malignant endocrine tumor. Differentiated thyroid cancer (DTC) accounts for 95% of thyroid cancer cases. The primary treatment for intermediate‑ and high‑risk DTC is total thyroidectomy....
Thyroid cancer is the most common malignant endocrine tumor. Differentiated thyroid cancer (DTC) accounts for 95% of thyroid cancer cases. The primary treatment for intermediate‑ and high‑risk DTC is total thyroidectomy. Postoperatively, serum thyroglobulin (Tg) and anti‑Tg antibody (Tg/Ab) levels are monitored to detect residual, recurrent or metastatic disease. Radioactive iodine (I) therapy is administered orally when Tg and Tg/Ab levels exceed standard levels. Recombinant human thyroid‑stimulating hormone (rhTSH) administration methods that do not require thyroid hormone withdrawal treatment and hospitalization have been recommended. However, serum Tg levels, a biomarker of thyroid tissue ablation, are often disturbed by Tg/Ab interference, which is observed in one‑quarter of patients with DTC. The present study aimed to elucidate the molecular mechanisms underlying metabolic changes in patients with DTC treated with I, and to identify Tg/Ab‑independent biomarker candidates using the TPC‑1 cell model. Blood serum samples were collected from patients with DTC before and after administration of I, which was performed following stimulation with rhTSH. Intra‑individual variations in Tg and Tg/Ab levels were observed in the same patients before and after I administration. Serum metabolomic analysis showed elevated levels of branched‑chain amino acid (BCAA), including valine, leucine and isoleucine, in all 3 patients, who exhibited favorable clinical outcomes. Although the number of cases was limited, this may suggest a possible association between BCAA levels and treatment response. Additionally, while overall boronophenylalanine uptake decreased in the total cell population after ionizing radiation exposure, the surviving viable TPC‑1 cells exhibited relatively increased amino acid uptake, assessed using boronophenylalanine as a leucine analog, which corresponded to the findings presented in the cell‑based experiments. Higher expression levels of the CD98 cell surface antigen were observed in irradiated TPC‑1 cells compared with non‑irradiated controls, which may contribute to increased uptake of BCAAs. However, the mRNA expression levels of L‑type amino acid transporter type 1 (), L‑type amino acid transporter type 2 and did not change upon exposure to IR. These results indicated that the increased BCAA uptake in IR‑exposed DTC cells was a transient response likely mediated by LAT1/CD98hc at the cell surface, as suggested by flow cytometry analysis, despite no corresponding increase in mRNA expression.
[Retracted] Effects and mechanisms of fatty acid metabolism‑mediated glycolysis regulated by betulinic acid‑loaded nanoliposomes in colorectal cancer.
Wang G, Yu Y, Wang YZ … +3 more , Zhu ZM, Yin PH, Xu K
Oncol Rep · 2025 Dec · PMID 40999969 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the western blot experiments shown in Figs. 6E and 7C, a pair of the gel slices were strikingly simila...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the western blot experiments shown in Figs. 6E and 7C, a pair of the gel slices were strikingly similar in appearance, suggesting that the same data had been included in these figures to show the results with different proteins. Moreover, two additional gel slices in these figures had apparently been re‑used in a pair of subsequent papers published by the same research group, where the experimental conditions were indicated to be different, and it was noted by the Editorial Office that one of the gel slices may have contained an anomaly in the form of a break in the continuity of the gel. Upon asking the authors to provide the Editorial Office with an explanation of the above issues, they did supply us with revised versions of Figs. 6E and 7C; however, it was subsequently pointed out to the authors that certain of the western blot data in Fig. 6E had apparently reappeared in a further paper by the same authors, in the journal . Owing to the lack of a further response from the authors in relation to the latter query, the Editor of has decided that this paper should now 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. [Oncology Reports 44: 2595‑2609, 2020; DOI: 10.3892/or.2020.7787].
[Expression of Concern] Reciprocal negative feedback loop between EZH2 and miR‑101‑1 contributes to miR‑101 deregulation in hepatocellular carcinoma.
Huang D, Wang X, Zhuang C … +5 more , Shi W, Liu M, Tu Q, Zhang D, Hu L
Oncol Rep · 2025 Dec · PMID 40999965 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell assay data shown in Fig. 5B on p. 1088, the rightmost panels in the top and the bottom rows ap...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell assay data shown in Fig. 5B on p. 1088, the rightmost panels in the top and the bottom rows appeared to contain a small overlapping section, suggesting that data which were intended to show the results of differently performed experiments had been derived from the same original source. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper; however, 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 continues to investigate this matter further. [Oncology Reports 35: 1083‑1090, 2016; DOI: 10.3892/or.2015.4467].
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