Oncology reports最新文献

Glioblastoma remains a lethal malignancy with limited therapeutic advancements. Emerging evidence implicates cell cycle dysregulation in glioma pathogenesis, yet the mechanistic role of cyclin‑dependent kinase 1 (CDK1) remains underexplored. The present study systematically evaluated the clinical relevance and functional impact of CDK1 in glioma progression through multi‑modal experimental approaches. CDK1 expression was analyzed using public datasets and then verified by western blotting using patient tissue samples (n=37) from the Second Hospital of Hebei Medical University (Shijiazhuang, China). Survival analysis was performed using Chinese Glioma Genome Atlas and The Cancer Genome Atlas datasets, alongside multivariate Cox regression to evaluate prognostic independence. Functional assays, including small interfering RNA‑mediated CDK1 knockdown, were conducted in glioma cell lines to assess proliferation (Cell Counting Kit‑8 and EdU), migration/invasion (Transwell), apoptosis (acridine orange/ethidium bromide staining and flow cytometry) and radiosensitivity (γ‑H2AX foci quantification post‑irradiation). The expression levels of downstream cell cycle regulators were quantified via quantitative PCR. The results indicated that CDK1 was significantly upregulated in glioma tissues compared with normal controls, with expression levels escalating with tumor grade. High CDK1 expression correlated with a reduced overall survival and served as an independent prognostic marker. CDK1 knockdown attenuated glioma cell proliferation, migration and invasion, while enhancing apoptosis and radiosensitivity. Mechanistically, CDK1 knockdown downregulated cell cycle regulators proliferating cell nuclear antigen, minichromosome maintenance complex component 2‑4 (MCM2‑4), MCM6, polo‑like kinase 1, TTK protein kinase and mitotic arrest deficient 2 like 1, implicating mitotic dysregulation as a central pathway. The present study established CDK1 as a master regulator of glioma progression through coordinated control of proliferation, DNA repair and metastatic potential. The robust association between CDK1 expression, tumor grade and survival, coupled with functional validation across complementary assays, positions CDK1 inhibition as a promising therapeutic strategy. The mechanistic elucidation of its cell cycle network provides a novel framework for targeting glioma‑specific therapeutic targets.

Following the publication of the above article, the authors contacted the Editorial Office to explain that they had made inadvertent errors in compiling a couple of the figures in the above paper; first, regarding the immunohistochemical images shown in Fig. 2D on p. 5, the data panel shown correctly for the 'LC3/TPL+DDP' experiment contained an overlapping section with the 'LC3/TPL' data panel in the same figure part (the latter of which had been incorporated into this figure incorrectly). Secondly, the β‑actin bands correctly shown in Fig. 3D on p. 6 had incorrectly been included to represent the JAK2 western blot data in Fig. 4F on p. 7. However, the authors were able to re‑examine their original data, and realized how these errors had occurred. The revised and corrected versions of Figs. 2 and 4, now showing the correct data for the 'LC3/TPL' experiment in Fig. 2D and the JAK2 western blot data in Fig. 4F, are shown on the next two pages. Note that the errors made with the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors apologize to the Editor of Oncology Reports and to the readership for any inconvenience caused. [Oncology Reports 45: 69, 2021; DOI: 10.3892/or.2021.8020]

Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations are among the most frequent oncogenic drivers in cancer, particularly in non‑small cell lung cancer (NSCLC). KRAS was previously considered an 'undruggable' target due to the protein's smooth molecular surface and the absence of obvious drug binding sites. However, the development of selective KRAS G12C inhibitors, such as sotorasib and adagrasib, together with progress in immunotherapy, have demonstrated potential clinical activity. Further understanding of the complex signaling networks driven by KRAS has revealed new opportunities to target this pathway directly or through rational combination strategies. The present review explored KRAS‑targeted therapies and immunotherapies, including limitations, resistance mechanisms and the efficacy of combination regimens. Although there has been notable progress, concerns regarding optimal therapy combinations, resistance management and early treatment strategies remain. The present review demonstrated the need for continued research to address these challenges and improve outcomes for patients with KRAS‑mutated NSCLC.

Lung cancer remains a significant global health challenge, with metastatic progression being the leading driver of mortality. Organoid technology provides a tractable, physiologically relevant platform to model key aspects of lung cancer metastasis in vitro. The present review summarized methodologies for constructing and interrogating these models, covering tissue sources, culture modalities, gene editing and in vivo transplantation; applications in studying metastatic mechanisms, drug screening and capturing intra‑ and intertumoral heterogeneity are also highlighted. Persistent challenges include standardizing derivation and culture conditions, improving preservation of tumor‑microenvironmental interactions, expanding immune‑competent and vascularized models, and addressing scalability, cost, and regulatory and ethical considerations for clinical translation. Future directions include integrating multi‑omics approaches and spatial profiling, leveraging artificial intelligence for image and response analytics, advancing immune‑organoid models and establishing shared standards, reference materials and reporting guidelines to enhance reproducibility and clinical impact.

Subsequently to the publication of the above paper, a concerned reader has drawn to the Editor's attention that, for the immunohistochemical data shown in Fig. 2E, the same data panel had apparently been included for the 'ZEB1/Con' and 'SEB2/Min' experiments. In addition, for the Snail2 experiments shown in Fig. 3A, the Snail Con(trol) and Snail Mimi panels looked strikingly similar, even though the intensity of the antibody (red) channel appeared to have been decreased in the Mimi panel. Finally, for the immunohistochemical images shown in Fig. 3C, the E‑cadherin Con(trol) and Scr panels appeared to show a region of overlap, suggesting that these data were derived from the same original source, where the results of differently performed experiments were intended to have been portrayed. Given that it has come to light that this trio of figures had apparently been assembled incorrectly, which might have had an adverse effect on the interpretation of the results and conclusions in the article, the Editor of Oncology Reports 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 29: 1579‑1587, 2013; DOI: 10.3892/or.2013.2267]

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.

Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, concerning the cell migration and invasion assay experiments shown in Figs. 3 and 4, the 'WT/Migration' and 'Ctrl/Invasion' panels in Fig. 3C contained an overlapping section of data, and the 'WT/Invasion' and 'CXCR-sh/Migration' panels in Fig. 4A were duplicates, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original sources. Upon examining the data independently in the Editorial Office, it also came to light that the  E-cadherin western blot in Fig. 3E was strikingly similar to the N-cadherin western blot shown in Fig. 4A. However, the authors were able to consult their original data, and recognized that these data had inadvertently been included in these two figures incorrectly. Revised and corrected versions of Figs. 3 and 4, now showing the correct data for the E-cadherin blot in Fig. 3E and the 'Ctrl/Invasion' experiment in Fig. 3C, and the 'CXCR-sh/Migration' panel in Fig. 4A, are shown on the next page. The authors regret the errors that were made during the compilation of the original figures, and are grateful to the editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum. Note that these errors did not have a significant impact on the conclusions reached in this study. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the readership for any inconvenience caused. [Oncology Reports 37: 3279-3286, 2017; DOI: 10.3892/or.2017.5598].

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 Oncology Reports 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].

Primary cilia are antenna‑like organelles on almost all human cells that sense and transduce extracellular cues into cellular response. Primary cilia have been reported to be implicated in drug resistance in several cancer types, but their roles in cellular response to epidermal growth factor receptor (EGFR)‑tyrosine kinase inhibitors (TKIs) in non‑small cell lung cancer (NSCLC) are still not fully understood. In the present study, it was reported that primary cilia are more prevalent in EGFR‑TKI‑insensitive A549 and H23 cells compared with the drug‑sensitive HCC827 and PC9 cells by immunofluorescence staining assay. Importantly, treatment with EGFR‑TKIs (gefitinib and dacomitinib) results in a dose‑dependent increase in cilia number and length in A549 and H23 cells, an effect not observed in HCC827 and PC9 cells. Upon administration of gefitinib, A549 cells predominantly arrest in the G1 phase detected by flow cytometric analysis, with a minority undergoing cell death and the majority entering senescence. Inhibition of ciliogenesis through the knockdown of IFT88 or ARL13B by targeted small interfering RNAs markedly enhances the sensitivity of A549 cells to EGFR‑TKIs by promoting a shift from senescence to cell death. Furthermore, it was demonstrated by immunoblotting and immunofluorescence colocalization analysis that both the expression and ciliary localization of adenylate cyclase 3 (AC3) are significantly upregulated following EGFR‑TKIs treatment, and the reduction of AC3 expression effectively mitigates cellular drug resistance in A549 cells. These findings highlight a critical role for the cilia‑AC3 axis in modulating cellular response to EGFR‑TKIs, suggesting it as a potential therapeutic target for the treatment of NSCLC.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that areas of the cellular images shown in Fig. 3A and B appeared to be identical to data shown in Fig. 1 of an article published in Journal of Molecular Neuroscience a year earlier (in 2012) by the same research group, although in that case, these data were used to represent different experiments. Moreover, comparing the two publications, for the same data, the bar charts showing the 'number of migrating BMSCs' reported very different average measurements (~38 in the Journal of Molecular Neuroscience paper, and ~220 in the paper above). Owing to the fact that the abovementioned data had been re‑used in the above paper in an unrelated experimental context, the Editor of Oncology Reports 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 30: 2755‑2764, 2013; DOI: 10.3892/or.2013.2780].