Oncol. Rep. [JOURNAL]
Sun
200 papers
Liquid biopsy in malignant primary bone tumors: Clinical applications of circulating tumor DNA and circulating tumor cells for diagnosis, prognosis and treatment monitoring (Review).
Tian B, Chen X, Zheng J … +1 more , Kang X
Oncol Rep · 2026 Apr · PMID 41685600 · Full text
Liquid biopsy, which involves the detection of circulating tumor DNA (ctDNA) and circulating tumor cells (CTCs), is revolutionizing the management of osteosarcoma, Ewing sarcoma and chondrosarcoma by enabling noninvasive...
Liquid biopsy, which involves the detection of circulating tumor DNA (ctDNA) and circulating tumor cells (CTCs), is revolutionizing the management of osteosarcoma, Ewing sarcoma and chondrosarcoma by enabling noninvasive diagnosis, risk stratification and real‑time treatment monitoring. ctDNA analysis allows for the sensitive detection of tumor‑specific alterations, whereas CTCs provide insights into metastatic potential. Baseline ctDNA burden independently predicts poor survival, while dynamic ctDNA kinetics and CTC counts guide neoadjuvant response assessment and postoperative minimal residual disease surveillance. Notably, the integration of liquid biopsy into adaptive clinical pathways can refine precision oncology for these rare, lethal bone malignancies.
Tumor visualization and evaluation of glioblastoma in mice using small animal 9.4T MRI and PET‑CT with high resolution.
Li S, Gu W, Jiang Y … +11 more , Liu T, Shuai L, Wei Y, Shi Y, Juvenal H, Wang Z, Wei Y, Wu B, Zhou X, Li Y, Tang F
Oncol Rep · 2026 Apr · PMID 41685597 · Full text
Glioblastoma (GBM) is the most prevalent type of malignant primary brain tumor. Preclinical research serves a key role in investigating the development and mechanism of GBM tumor. However, the dynamic and non‑invasive ev...
Glioblastoma (GBM) is the most prevalent type of malignant primary brain tumor. Preclinical research serves a key role in investigating the development and mechanism of GBM tumor. However, the dynamic and non‑invasive evaluation of tumors in animals faces challenges, such as the limited sensitivity of clinical instruments and insufficient spatial resolution for mouse brain tumors. The present study aimed to establish an mouse GBM model and evaluate the model using high resolution small animal positron emission tomography‑computed tomography (PET‑CT) and magnetic resonance imaging (MRI). Metabolism was compared between the normal brain and tumor tissue by using H‑magnetic resonance spectroscopy (H‑MRS). T2‑weighted imaging (T2WI) MRI detected the tumor in the brain 7 days after injection of GL261 cells, with tumor sizes of 1.263, 4.917 and 13.85 mm on days 7, 14 and 21, respectively. H‑MRS demonstrated that the levels of tissue metabolites such as lactate and total choline increased, while those representing neurological function of the brain such as total N‑acetylaspartate decreased in tumor compared with the normal brain tissues. PET‑CT imaging confirmed the tumor detected by MRI. At 6‑120 min post F‑fluorodeoxyglucose (FDG) administration, the standard uptake value (SUV) in tumor tissue gradually increased, while the SUV value in normal brain tissue gradually decreased. SUV in the liver and kidneys decreased, while SUV in the bladder increased in a time‑dependent manner. Pharmacokinetic analysis showed that the distribution of FDG in brain and tumor tissue conformed to a two‑tissue compartment model. This model consists of a plasma compartment and two tissue compartments representing free FDG and phosphorylated FDG within brain or tumor tissue. The model parameters are defined as follows: Fractional blood volume (vB)=3.6%, k1 (forward transport rate)=1.844, k2 (reverse transport rate)=3.844 and k3 (phosphorylation rate)=0.280 in brain and vB=2.3%, k1=0.797, k2=2.722 and k3=0.319 in tumor tissue, respectively. The tumors observed by MRI and PET‑CT imaging were ultimately confirmed through morphological and pathological analysis. Compared with normal brain tissue, glioma tissue exhibited significantly elevated glucose transporter type 1 protein levels. In conclusion, the model was confirmed by high‑resolution small animal PET‑CT and MRI, as well as morphological and pathological approaches.
[Expression of Concern] Interference of STAT 5b expression enhances the chemo‑sensitivity of gastric cancer cells to gefitinib by promoting mitochondrial pathway‑mediated cell apoptosis.
Sun T, Jia Y, Xiao D
Oncol Rep · 2026 Apr · PMID 41685596 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the β‑actin blots for the MGC‑803 cell line in Fig. 4A were strikingly similar to the blots on the right‑han...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the β‑actin blots for the MGC‑803 cell line in Fig. 4A were strikingly similar to the blots on the right‑hand side of the gel intended to show the caspase‑9 experiments in Fig. 7A; moreover, the blots shown for caspase‑3 for the MGC‑803 cell line in Fig. 4A were remarkably similar to blots that subsequently appeared in another article featuring one of the named authors (Tao Sun) in the same journal about a year later. In addition, a number of duplicated blots were noted comparing the flow cytometric plots in Figs. 3 and 6, including one blot which subsequently reappeared in a paper published in the journal that was written by different authors. The authors were contacted by the Editorial Office to offer an explanation for the apparent duplications of data both within the paper, and the subsequently published ones. 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. [Molecular Medicine Reports 34: 227‑234, 2015; DOI: 10.3892/or.2015.3994].
[Corrigendum] Hypoxia and macrophages promote glioblastoma invasion by the CCL4‑CCR5 axis.
Wang Y, Liu T, Yang N … +3 more , Xu S, Li X, Wang D
Oncol Rep · 2026 Apr · PMID 41645763 · Full text
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, in comparing Figs. 1A and 2B, which both showed the results of invasion assay experiments, the 'Normoxia / U87...
Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, in comparing Figs. 1A and 2B, which both showed the results of invasion assay experiments, the 'Normoxia / U87' data panel in Fig. 1A appeared to overlap with the 'CCR5 siRNA' panel in Fig. 2B, whereas the 'Hypoxia / U87‑Mφ' panel in Fig. 1A also appeared to overlap with the 'Control siRNA' panel in Fig. 2B [also note that an expression of concern statement (doi.org/10.3892/or.2025.8989) was issued for this paper]. The authors were able to re‑examine their original data files, and realized that the images for Fig. 2B had been inadverently selected incorrectly. The revised version of Fig. 2, containing the correct data for the invasion assay experiments in Fig. 2B, is shown on the next page. Note that the corrections made to this figure do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [Oncology Reports 36: 3522‑3528, 2016; DOI: 10.3892/or.2016.5171].
Quercetin reduces expression of ATP‑binding cassette transporters by regulating the PTEN/PI3K/AKT signaling pathway in breast cancer cells.
Fu W, Lin L, Li J … +7 more , Qin F, Chen C, Cai Y, Cai Y, Huang Y, Yang W, Zhu S
Oncol Rep · 2026 Apr · PMID 41645759 · Full text
Breast cancer is a global health challenge for women and chemoresistance is a major contributor to its high mortality rates. Quercetin (Que), a flavonoid with antioxidant, antiviral, anti‑tumor and anti‑inflammatory prop...
Breast cancer is a global health challenge for women and chemoresistance is a major contributor to its high mortality rates. Quercetin (Que), a flavonoid with antioxidant, antiviral, anti‑tumor and anti‑inflammatory properties, sensitizes cancer cells to chemotherapy. The present study investigated the mechanism by which Que regulates ATP‑binding cassette (ABC) transporter expression in MCF‑7 cells using a PTEN overexpression plasmid and the PI3K inhibitor LY294002. The present study assessed cell viability via Cell Counting Kit‑8 and Hoechst 33342 staining and analyzed mRNA and protein expression levels by reverse transcription‑quantitative PCR and western blotting. Apoptosis was evaluated by flow cytometry and ABCG2 expression was detected by immunofluorescence. Furthermore, the present study determined the effect of Que on drug uptake using a Rhodamine 123 accumulation assay. The results of the present study demonstrated that Que suppresses cell viability and induces apoptosis in MCF‑7 cells. Moreover, it enhances intracellular drug accumulation and downregulates ABC transporter expression by modulating the PTEN/PI3K/AKT signaling pathway.
POSTN fibroblast‑secreted small extracellular vesicles drive macrophage M2 polarization through BMP4/BMPR2/Smad signaling.
Zhang C, Chen S, Qian C … +5 more , Lv W, Zhang Q, Wang Y, Wu Y, Liu X
Oncol Rep · 2026 Apr · PMID 41645751 · Full text
Carcinoma‑associated fibroblasts (CAFs) exhibit notably heterogeneity and are closely implicated in immune checkpoint blockade (ICB) resistance in head and neck squamous cell carcinoma (HNSCC). However, the specific subt...
Carcinoma‑associated fibroblasts (CAFs) exhibit notably heterogeneity and are closely implicated in immune checkpoint blockade (ICB) resistance in head and neck squamous cell carcinoma (HNSCC). However, the specific subtypes and mechanisms involved remain to be elucidated. By analyzing two single‑cell RNA sequencing datasets (GSE103322 and GSE139324) and The Cancer Genome Atlas (TCGA)‑HNSCC dataset, two distinct fibroblasts subtypes were identified: Perostin (POSTN) and POSTN fibroblasts. A comparison with reported markers revealed that extracellular matrix‑related markers were highly expressed in POSTN fibroblasts. In addition, fibroblast activation protein and POSTN expression were positively associated with macrophage infiltration and predicted ICB resistance in TCGA‑HNSCC dataset. Immunogold labeling confirmed the enrichment of POSTN on the membrane surface of CAF‑derived small extracellular vesicles (sEVs) and it was indicated that these POSTN sEVs may promote THP‑1‑derived macrophages polarization toward the M2 phenotype. Additionally, sEVs derived from CAFs with POSTN knockdown reduced bone morphogenetic protein (BMP) 4 expression in macrophages, thereby inhibiting M2 polarization through the BMP receptor 2/Smad pathway. Collectively, these findings revealed that a POSTN fibroblasts fosters an immunosuppressive microenvironment via sEV‑mediated macrophage polarization, nominating POSTN as a potential therapeutic target to overcome ICB resistance in HNSCC.
[Retracted] EGFR/HER2 inhibitors effectively reduce the malignant potential of MDR breast cancer evoked by P‑gp substrates and .
Jin Y, Zhang W, Wang H … +4 more , Zhang Z, Chu C, Liu X, Zou Q
Oncol Rep · 2026 Apr · PMID 41645745 · Full text
Following the publication of the above article, it was drawn to our attention by a concerned reader that the pairs of data panels showing the results for the Paxitaxel (or Epirubicin) + Lapatinib and the Paxitaxel (or Ep...
Following the publication of the above article, it was drawn to our attention by a concerned reader that the pairs of data panels showing the results for the Paxitaxel (or Epirubicin) + Lapatinib and the Paxitaxel (or Epirubicin) + Trastuzumab experiments respectively in Fig. 2E on p. 774 were overlapping, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original sources. After having further investigated the data in this paper in the Editorial Office, it was also identified that certain Transwell assay data were shared comparing Fig. 1D with Fig. 2E, and several of the western blot control experimental data were shared between Figs. 1A‑C and 2A‑C, although it wasn't entirely clear whether these data were intended to have portrayed the same experimental results in these figures. More importantly, examining the immuno-histochemical assay data in Fig. 3A and B, two pairs of data panels were found to be overlapping, where these figure parts were described in the legend as relating to mouse and human experiments respectively; therefore, different experimental data presumably should have been presented for Fig. 3A and B in this figure. The authors requested that a corrigendum be published to present the data in Fig. 2 (initially) accurately. The Editor of has considered the authors' request to publish a corrigendum, but has decided to decline this request on account of the additional errors that have been identified in the assembly of data in (at least) Fig. 3 in this paper; rather, the article is to be be retracted from the Journal on account of an overall lack of confidence in the presented data. The authors were asked for an explanation to account for these additional concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership of the Journal for any inconvenience caused. [Oncology Reports 35: 771‑778, 2016; DOI: 10.3892/or.2015.4444].
Tumor‑associated glucocorticoid inhibition by mifepristone reduces polymorphonuclear myeloid‑derived suppressor cells and promotes antitumor immunity in triple‑negative breast cancer‑bearing mice.
Kobayashi M, Konno C, Shimizu A … +2 more , Kobayashi M, Hori T
Oncol Rep · 2026 Apr · PMID 41645739 · Full text
Triple‑negative breast cancer (TNBC) is a highly malignant subtype with limited effective treatment options. The present study investigated the antitumor immune effects of mifepristone, a glucocorticoid receptor antagoni...
Triple‑negative breast cancer (TNBC) is a highly malignant subtype with limited effective treatment options. The present study investigated the antitumor immune effects of mifepristone, a glucocorticoid receptor antagonist, using subcutaneous, orthotopic and experimental lung metastasis mouse models transplanted with 4T1 TNBC cells. Mifepristone treatment suppressed tumor growth and metastasis, leading to improved overall survival. Flow cytometric analysis of the spleen revealed decreased polymorphonuclear myeloid‑derived suppressor cells (PMN‑MDSCs) and increased T cells in the spleen, accompanied by enhanced T‑cell activity assessed . Similar immune alterations were observed in tumor‑infiltrating cells, indicating enhanced intratumoral T‑cell responses. These results suggested that the antitumor effects of mifepristone may be partly mediated by reducing PMN‑MDSCs and restoring antitumor immunity. In tumor‑bearing mice, plasma levels of corticosterone, the major murine glucocorticoid, were elevated. In experiments using bone marrow and splenocytes, corticosterone promoted PMN‑MDSC induction and suppressed T‑cell activity, and these effects were reversed by mifepristone. Thus, mifepristone may modulate immune cell dynamics by inhibiting systemic corticosterone. To elucidate the mechanism underlying plasma corticosterone elevation, the corticosterone‑generating capacity of 4T1 cells was analyzed by exposing them to 11‑dehydrocorticosterone (DHC). The results demonstrated that 4T1 cells possessed the ability to convert the inactive form of glucocorticoid, DHC, into its active form, corticosterone, through the enzymatic activity of 11β‑hydroxysteroid dehydrogenase type 1 (11β‑HSD1). Furthermore, treatment with carbenoxolone (a non‑selective 11β‑HSD1 inhibitor) in tumor‑bearing mice decreased plasma corticosterone levels, suppressed tumor growth and produced immune changes similar to mifepristone treatment. These findings suggested that the elevated plasma corticosterone levels in tumor‑bearing mice may be mediated by 11β‑HSD1‑dependent corticosterone production, and that this mechanism was likely induced by 4T1 cells. In conclusion, the present study indicated that 4T1 cells possess corticosterone‑generating capacity through 11β‑HSD1, promoting systemic corticosterone elevation and tumor growth. Mifepristone may restore antitumor immunity, likely by reducing PMN‑MDSCs through systemic corticosterone blockade. These insights could inform the development of novel therapeutic approaches for TNBC.
Origin dictates function: The dual roles of exosomes derived from diverse origins in the onset and progression of colorectal cancer (Review).
Guo Z, Zhuang H, Liu Q
Oncol Rep · 2026 Apr · PMID 41645735 · Full text
Globally, colorectal cancer (CRC) ranks third in terms of incidence, while it is the second leading cause of cancer‑related mortality. The high incidence and mortality rates of CRC pose a considerable challenge to global...
Globally, colorectal cancer (CRC) ranks third in terms of incidence, while it is the second leading cause of cancer‑related mortality. The high incidence and mortality rates of CRC pose a considerable challenge to global human health. Currently, surgical treatment and chemotherapy, which exert unsatisfactory clinical benefits in patients with CRC, are posing major issues in clinical practice, including recurrence, drug resistance and drug toxicity. Therefore, novel treatment approaches for CRC are urgently needed. Emerging evidence has suggested that exosomes carry out a key role in the occurrence and development of CRC, thus attracting considerable attention from researchers. However, exosomes act in a source‑dependent manner as exosomes from different sources can exhibit distinct roles in the onset and progression of CRC. The present review systematically summarizes the molecular mechanisms underlying the effects of exosomes from different sources on promoting or inhibiting CRC. Additionally, the potential of exosomes in the diagnosis and treatment of CRC are also discussed, thus providing a foundation for the future application of exosomes in managing CRC.
[Retracted] MicroRNA‑615‑5p targets insulin‑like growth factor 2 and exerts tumor‑suppressing functions in human esophageal squamous cell carcinoma.
Yang B, Xie R, Wu SN … +3 more , Gao CC, Yang XZ, Zhou JF
Oncol Rep · 2026 Apr · PMID 41614419 · Full text
Following the publication of the above article, a concerned reader drew to the Editor's attention that there were anomalies associated with the Transwell data shown in Figs. 2B and C and 5A‑D; essentially, groupings of c...
Following the publication of the above article, a concerned reader drew to the Editor's attention that there were anomalies associated with the Transwell data shown in Figs. 2B and C and 5A‑D; essentially, groupings of cells appeared to be markedly similar in appearance looking within various of the data panels in these figures. After having conducted an internal investigation of the data in this paper, the Editor of has judged that the potentially anomalous presentation of the strikingly similar groupings of cells in Figs. 2 and 5 were too extensive that these features could have been attributed to pure coincidence. Therefore, the Editor has decided that this article should be retracted from the publication on the grounds of an overall 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 incovenience caused, and we thank the reader for bringing this matter to our attention. [Oncology Reports 39: 255‑263, 2018; DOI: 10.3892/or.2017.6079].
TRIM46 deficiency‑induced DNA damage enhances the sensitivity of cisplatin in non‑small cell lung cancer by regulating the Akt signaling pathway.
Jin S, Zhang D, Liao Z … +6 more , Yu L, Wang Y, Jia P, Pan M, Li Y, Zhang J
Oncol Rep · 2026 Apr · PMID 41614410 · Full text
Lung cancer is one of the most aggressive malignancies worldwide. Non‑small cell lung cancer (NSCLC), in particular, is characterized by a poor 5‑year survival rate, which is largely attributable to cisplatin (DDP) resis...
Lung cancer is one of the most aggressive malignancies worldwide. Non‑small cell lung cancer (NSCLC), in particular, is characterized by a poor 5‑year survival rate, which is largely attributable to cisplatin (DDP) resistance. However, the molecular mechanisms underlying DDP resistance are still not fully understood. Tripartite motif 46 (TRIM46) is implicated in promoting the progression of lung adenocarcinoma and enhancing chemoresistance. Nevertheless, its specific role in DDP resistance remains elusive. The present study aimed to investigate the role of TRIM46 in DDP resistance. Immunohistochemistry and TUNEL staining were employed to detect the expression of TRIM46 and apoptotic cells in tumor tissues. Lentiviruses were used to construct TRIM46 overexpression and knockdown vectors in A549 and A549/DDP cells. Cell proliferation, apoptosis and DNA damage were measured by Cell Counting Kit‑8, flow cytometry and comet assay, respectively. Subcutaneous implantation model through injection of A549/DDP cells with TRIM46 knockdown was performed in BALB/c nude female mice, followed by DDP treatment. The results revealed that TRIM46 was highly expressed in DDP‑resistant NSCLC tumor tissues and positively associated with DDP resistance. TRIM46 overexpression attenuated the DDP‑induced apoptosis and DNA damage of A549 cells. Meanwhile, the knockdown of TRIM46 enhanced the DDP‑induced apoptosis and DNA damage in A549/DDP cells. Mechanistically, TRIM46 activated the Akt signaling, thus inhibiting the expression of caspase 3 and cleaved‑caspase 3 as well as increasing the expression level of DNA repair protein RAD51. Furthermore, TRIM46 deficiency inhibited tumor growth and increased DDP sensitivity . In conclusion, the results of the present study demonstrated that TRIM46 contributed to DDP resistance by regulating the Akt signaling pathway and DNA damage, thereby offering new strategies for lung cancer therapy.
Mitochondria in T‑cell tumor immunity and tumor therapies targeting mitochondria (Review).
Zhou M, Xie Y, Liu Z … +6 more , He Y, Yin Y, Chen K, Zhao Z, Zhang C, Cai D
Oncol Rep · 2026 Apr · PMID 41614403 · Full text
Mitochondria are central to cellular metabolic reprogramming, and their energy metabolism pathways are indispensable for T‑cell activation, proliferation and differentiation. Mitochondrial metabolic reprogramming enhance...
Mitochondria are central to cellular metabolic reprogramming, and their energy metabolism pathways are indispensable for T‑cell activation, proliferation and differentiation. Mitochondrial metabolic reprogramming enhances T‑cell activity and antitumor function. Mitochondrial dynamics, including fusion, fission and transfer, regulate T‑cell tumor immune function by modulating the number, morphology and distribution of mitochondria, which is vital for the antitumor effects of T cells. The release of mitochondrial DNA can activate multiple innate immune signaling pathways, such as cyclic GMP‑AMP synthase‑stimulator of interferon genes, Toll‑like receptor 9, and NOD‑, LRR‑, and pyrin domain‑containing protein 3, serving a complex regulatory role in shaping the tumor immunosuppressive microenvironment and T‑cell antitumor immune responses. Notably, mitochondrial dysfunction is a major driver of tumor initiation and progression. T‑cell mitochondrial metabolic reprogramming, dynamic changes and mitochondrial DNA release all affect the antitumor immunity of tumor‑infiltrating T cells. The present review focuses on the relationship between mitochondria and T‑cell antitumor immune responses, exploring the core role of mitochondria in T‑cell tumor immunity from multiple aspects, including mitochondrial energy metabolism, mitochondrial dynamics and mitochondrial DNA. In addition, the present review examines state‑of‑the‑art research on antitumor therapies targeting mitochondria from multiple perspectives, with the aim of providing a reference for developing mitochondria‑targeted antitumor immunotherapy strategies.
Advances in isolation and detection technologies and immunotherapy applications of circulating tumor cells (Review).
Zhou P, Ye Q, Huang Y … +3 more , Feng Y, Zhou L, Xie K
Oncol Rep · 2026 Apr · PMID 41614401 · Full text
Circulating tumor cells (CTCs) are shed from the primary tumor into the peripheral bloodstream, where they play crucial roles in tumor metastasis and recurrence. As a cornerstone of liquid biopsy, CTCs hold significant p...
Circulating tumor cells (CTCs) are shed from the primary tumor into the peripheral bloodstream, where they play crucial roles in tumor metastasis and recurrence. As a cornerstone of liquid biopsy, CTCs hold significant potential for early tumor diagnosis, therapeutic response monitoring, and prognosis. However, the rarity and heterogeneity of CTCs pose considerable challenges for their isolation and enrichment. Additionally, their predictive usefulness in tumor immunotherapy remains relatively limited. The present review summarizes recent advancements in CTC isolation and detection technologies, explores their clinical applications in immunotherapy, and discusses current challenges alongside potential strategies for improvement. The integration of these technologies into clinical practice could pave the way for more personalized and precise cancer treatment strategies in the future.
High RMI1 expression is associated with cancer cell progression and poor prognosis in prostate cancer.
Shen P, Wang X, Yan X … +3 more , Du H, Wu B, Cao X
Oncol Rep · 2026 Apr · PMID 41614397 · Full text
DNA replication stress and energy homeostasis are critical yet underexplored pathways in prostate cancer (PCa). Identifying PCa prognostic biomarkers associated with these pathways are essential for advancing diagnostics...
DNA replication stress and energy homeostasis are critical yet underexplored pathways in prostate cancer (PCa). Identifying PCa prognostic biomarkers associated with these pathways are essential for advancing diagnostics and treatment. The present study aimed to analyze transcriptomic and clinical data from public datasets to identify DNA replication stress and energy homeostasis‑related genes associated with PCa. Biomarkers were assessed using reverse transcription‑quantitative (RT‑q) PCR, western blotting and consistent expression trends across datasets. Survival analyses evaluated the effect of biomarkers on clinical outcomes, while immune microenvironment changes and immunotherapy responses were evaluated. Mutation and drug sensitivity analyses explored genetic variations and chemotherapy efficacy. Functional assays, including cell proliferation, migration, RT‑qPCR and western blotting, confirmed biomarker roles in PCa progression. RecQ mediated genome instability 1 (RMI1) was identified as a novel biomarker, consistently upregulated in PCa tissues across datasets and experiments (P<0.05). High RMI1 expression was associated with worse survival outcomes, advanced clinical stages, immune escape and TP53 mutations. Enrichment analysis linked RMI1 to cell cycle, DNA replication and metabolic pathways. Functional assays revealed that RMI1 knockdown inhibited PCa cell proliferation and migration, suggesting its role in tumor progression. Additionally, high RMI1 expression was associated with resistance to certain chemotherapeutic agents, such as irinotecan. These results underscored RMI1 as a promising prognostic biomarker and a potential therapeutic target for the management of PCa. In conclusion, the present study identified RMI1 as a biomarker for the detection of PCa and may promote cancer cell progression by promoting proliferation and migration.
[Corrigendum] 3‑Bromopyruvate sensitizes human breast cancer cells to TRAIL‑induced apoptosis via the phosphorylated AMPK‑mediated upregulation of DR5.
Chen Y, Wei L, Zhang X … +8 more , Liu X, Chen Y, Zhang S, Zhou L, Li Q, Pan Q, Zhao S, Liu H
Oncol Rep · 2026 Apr · PMID 41614396 · Full text
Following the publication of the above article and a corrigendum (doi: 10.3892/or.2022.8264) that was published 3 years ago to resolve the issue of two sets of duplicated western blots in Fig. 3, an interested reader dre...
Following the publication of the above article and a corrigendum (doi: 10.3892/or.2022.8264) that was published 3 years ago to resolve the issue of two sets of duplicated western blots in Fig. 3, an interested reader drew to the authors' attention that, in Fig. 5b on p. 2441, the western blot data bands shown to represent the GRP78 and Bcl‑2 proteins in the MCF‑7 group were strikingly similar; furthermore, the β‑actin bands shown for the MDA‑MB‑231 group in Fig. 5c were strikingly similar to the β‑actin bands shown in Fig. 2c on p. 2439. After having re‑examined their original data, the authors realized that the figure parts in question were inadvertently assembled erroneously. The revised version of Fig. 5, now featuring the correct data for the GRP78 western blot bands for the MCF‑7 group in Fig. 5b and the β‑actin bands in Fig. 5c, is shown in the next page. Note that the errors made in assembling this figure did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of for granting them the opportunity to publish this; furthermore, they apologize to the readership for any inconvenience caused. [Oncology Reports 40: 2435‑2444, 2018; DOI: 10.3892/or.2018.6644].
[Corrigendum] Icaritin acts synergistically with epirubicin to suppress bladder cancer growth through inhibition of autophagy.
Pan XW, Li L, Huang Y … +8 more , Huang H, Xu DF, Gao Y, Chen L, Ren JZ, Cao JW, Hong Y, Cui XG
Oncol Rep · 2026 Mar · PMID 41574730 · Full text
Following the publication of the above article, the authors have contacted the Editorial Office to explain that they had noticed that, in Fig. 4 on p. 339, the same western blot data for the ATG5 protein had inadvertentl...
Following the publication of the above article, the authors have contacted the Editorial Office to explain that they had noticed that, in Fig. 4 on p. 339, the same western blot data for the ATG5 protein had inadvertently been included for the T24 and the BT5637 cell lines for the 72 h experiments (the lower panels of blots). However, the authors had retained their original data, and were able to identify how this error occurred. The revised version of Fig. 4, now showing the correct data for the ATG5 protein for the 72 h experiment with the BT5637 cell line, is shown on the next page. Note that this error did not affect the overall results and conclusions reported in the paper. The authors are grateful to the Editor of for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the readership of the journal for any inconvenience caused. [Oncology Reports 35: 334‑342, 2016; DOI: 10.3892/or.2015.4335].
Collaborative breakthroughs in precision diagnosis and treatment of nasopharyngeal cancer: Biomarker‑driven screening and endoscopic minimally invasive surgery reshape the new paradigm of early intervention (Review).
Jin E, Lin W, Zeng X
Oncol Rep · 2026 Mar · PMID 41574726 · Full text
The management of nasopharyngeal carcinoma (NPC), a malignancy with pronounced geographic prevalence in Southeast Asia, is undergoing a paradigm shift toward precision medicine driven by innovations in early detection an...
The management of nasopharyngeal carcinoma (NPC), a malignancy with pronounced geographic prevalence in Southeast Asia, is undergoing a paradigm shift toward precision medicine driven by innovations in early detection and minimally invasive therapy. Breakthroughs in Epstein‑Barr virus (EBV)‑based screening, such as CRISPR‑associated protein 12a (Cas12a) amplification‑free assays, P85 antibody profiling and T‑cell receptor sequencing, now achieve 97.9% sensitivity and 99.3% specificity, enabling ultra‑early risk prediction 6‑12 months before clinical diagnosis. These advances synergise with multimodal imaging techniques such as narrow‑band imaging and I‑scan virtual chromoendoscopy, which detect sub‑5 mm lesions with 90% sensitivity, revolutionizing screening protocols. Therapeutically, endoscopic nasopharyngectomy (ENPG) exemplifies precision oncology, achieving ≥90% negative resection margins and a 92.1% 5‑year survival rate in early‑stage NPC while preserving key functions (such as swallowing and hearing) and reducing radiotherapy‑related morbidity. Yet, it should be regarded as an indication‑bounded option for carefully selected T1‑T2 disease in experienced centers and does not constitute a universal substitute for radiotherapy. Persistent challenges, including tumor heterogeneity, limited access to advanced technologies in resource‑constrained regions and restrictive ENPG eligibility, underscore the need for artificial intelligence‑driven multi‑omics risk models, portable diagnostic tools and multinational trials to validate long‑term outcomes. By integrating surgical‑immune synergy (such as neoadjuvant programmed cell death protein 1 inhibitors) and equitable implementation strategies, NPC care is transitioning from empirical approaches to a precision framework targeting >80% early diagnosis and >90% functional preservation, offering a roadmap to mitigate the global burden of this regionally concentrated cancer.
Epigenetic mechanisms and therapeutic advances in diffuse midline glioma (Review).
Wu W, Chen W, Ma W … +1 more , Wang Y
Oncol Rep · 2026 Mar · PMID 41574724 · Full text
Gliomas are the most common primary malignant tumors of the central nervous system in adults, with diffuse midline gliomas (DMG) being particularly aggressive and associated with inferior survival rate. Notwithstanding a...
Gliomas are the most common primary malignant tumors of the central nervous system in adults, with diffuse midline gliomas (DMG) being particularly aggressive and associated with inferior survival rate. Notwithstanding advances in molecular diagnostics and epigenetics, the specific pathological mechanisms of DMG remain to be fully elucidated. A series of studies have demonstrated that histone modifications, particularly the histone H3 lysine 27 (H3K27)M mutation, play a pivotal role in the development and progression of DMG. The mutation disrupts histone methylation and acetylation to induce widespread gene expression abnormalities, tumor aggressiveness and treatment resistance. Conventional treatments such as surgery, local radiotherapy and chemotherapy offer limited efficacy. However, emerging precision therapies targeting histone mutations, epigenetic modifications and innovative immunotherapies show promise in improving outcomes. The present study provided a comprehensive overview of the molecular mechanisms, epigenetic characteristics and the latest therapeutic advances in DMG. By investigating the H3K27M mutation and its associated epigenetic mechanisms, the present review aimed to establish theoretical frameworks and research avenues for developing precise therapeutic strategies for DMG, thus contributing to advancing the field of personalized medicine.
[Retracted] Prognostic significance of miR‑218 in human hepatocellular carcinoma and its role in cell growth.
Tu K, Li C, Zheng X … +3 more , Yang W, Yao Y, Liu Q
Oncol Rep · 2026 Mar · PMID 41574723 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data shown in Fig. 3C, the immunohistochemical data shown in Fig. 4B and the...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data shown in Fig. 3C, the immunohistochemical data shown in Fig. 4B and the western blots in Fig. 5B had already been submitted to, or were published in, articles in other journals that featured some of the same authors; moreover, some of these data subsequently appeared in different articles in other journals that were not connected with either this research group or this research topic. Upon investigating these issues further in the Editorial Office, it was noted that, concerning Figs. 3‑5 and as far as those papers sharing some of the same authors was concerned, the cases of data sharing weren't necessarily as simple as the data merely being duplicated. Given the sharing of these contentious data across a number of different journals, the Editor of has decided that this paper 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. [Oncology Reports 32: 1571‑1577, 2024; DOI: 10.3892/or.2014.3386].
Key immune cells in the tumor immune microenvironment of colorectal cancer: Roles and research advances (Review).
Qiu M, Lan C, Lin M … +1 more , Ma H
Oncol Rep · 2026 Mar · PMID 41574721 · Full text
Colorectal cancer (CRC) is the third most common cancer globally and the second leading cause of cancer‑related mortalities. Surgery‑centered multimodal therapy remains the cornerstone of care, yet outcomes are poor in a...
Colorectal cancer (CRC) is the third most common cancer globally and the second leading cause of cancer‑related mortalities. Surgery‑centered multimodal therapy remains the cornerstone of care, yet outcomes are poor in advanced or drug‑resistant disease. The tumor immune microenvironment (TIME), a network of immune cells, cytokines and stromal elements, shapes antitumor immunity and can either restrain or encourage tumor growth. Specific immune cells within the TIME influence CRC biology, while immune‑checkpoint blockade has delivered notable benefits, especially in microsatellite instability‑high tumors. The present review discusses the principal immune cell populations in the CRC TIME, outlines their mechanisms of action and discusses emerging cell‑based immunotherapies that may guide future precision treatment.
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