Oncology reports最新文献

Cholangiocarcinoma (CCA) is an aggressive malignancy with poor prognosis and a limited number of treatments is available. Disulfidptosis, a newly identified form of cell death triggered by disulfide bond accumulation during glucose deprivation, may influence cancer progression but its role in CCA is poorly understood. The present study investigated disulfidptosis‑related genes (DRGs) and their impact on CCA prognosis and immune modulation. Differential expression analysis of 100 DRGs using RNA sequencing data from The Cancer Genome Atlas and EMBL‑EBI identified 74 dysregulated genes in CCA. Unsupervised clustering stratified patients with CCA into two distinct subtypes (Subs): i) SubA; and ii) SubB. A four‑gene prognostic signature was developed using least absolute shrinkage and selection operator regression and validated via Kaplan‑Meier survival analysis and receiver operating characteristic curves. Immune infiltration and tumor microenvironment were evaluated using Cell‑type Identification by Estimating Relative Subsets of RNA Transcripts, Estimation of Stromal and Immune cells in Malignant Tumor tissues using Expression data and single‑sample Gene Set Enrichment Analysis. Functional assays, including small interfering RNA knockdown of CD109 and EFNB2 in CCA cell lines were used to investigate proliferation, migration, invasion and F‑actin staining. Results showed SubB, associated with higher disulfidptosis activity, had worse prognosis, increased immune cell infiltration and elevated immune checkpoint gene expression. The four‑gene signature effectively stratified patients into risk groups. Knockdown of CD109 and EFNB2 significantly suppressed CCA cell proliferation, migration and invasion while it promoted disulfidptosis under glucose deprivation. The present study established an association between DRGs and CCA prognosis/immune dynamics, provided a robust four‑gene prognostic signature, and identified CD109 and EFNB2 as potential therapeutic targets, positioning disulfidptosis as a promising focus for precision medicine in CCA.

Esophageal cancer is a highly prevalent malignancy worldwide. Although immunotherapy, particularly programmed cell death‑1/programmed cell death ligand 1 (PD‑1/PD‑L1) inhibitors, has notably improved patient outcomes, the overall response rate remains limited. This limited efficacy is largely attributed to complex immunosuppressive networks within the tumor microenvironment (TME). The present review systematically dissects the multifaceted regulatory mechanisms of the PD‑1/PD‑L1 signaling axis in the TME of esophageal squamous cell carcinoma (ESCC), and its impact on immunotherapeutic efficacy. Emerging evidence indicates that multiple immunosuppressive mechanisms within the TME shape the response to immune checkpoint inhibitors: Regulatory T cells enhance immunosuppression via the TGF‑β‑PD‑1/PD‑L1 axis; IL‑6/STAT3 signaling upregulates PD‑L1 expression and mitochondrial remodeling and amino acid network regulation exacerbate T cell exhaustion. Meanwhile, tertiary lymphoid structure (TLS) maturation is positively associated with clinical prognosis by promoting tissue‑resident memory T cell activation and enhancing antitumor immunity. By contrast, the predictive value of tumor mutational burden (TMB) is constrained by TME heterogeneity. Emerging strategies highlight the predictive potential of TLS maturity and TMB, although the predictive relevance of TMB in ESCC remains inconsistent. Combination approaches show promise in reversing T/natural killer cell exhaustion and remodeling immunosuppressive TMEs. Future research should combine multi‑omics data with clinical information to develop personalized immunotherapy models for ESCC.

Following the publication of this paper, and the publication of an Expression of Concern statement (doi.org/10.3892/or.2025.8979), the authors have replied concerning an issue that was drawn to our attention by an interested reader; namely, that the immunohistochemical images shown in Figs. 1E and 5E appeared to show an overlapping section, even though Figs. 1 and 5 were intended to show the results of SHP2 and Ras expression experiments, respectively. The authors were able to check their data, and realized that Fig. 5 had inadvertently been assembled incorrectly. The revised version of Fig. 5, now showing the correct data for Fig. 5E, is shown below. Note that these errors did not adversely affect either the results or the overall conclusions reported in this study. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of Oncology  Reports for allowing them the opportunity to publish this. They also wish to apologize to the readership of the Journal for any inconvenience caused. [Oncology  Reports 39: 611‑618, 2018; DOI: 10.3892/or.2017.6109.

Ferroptosis is a type of programmed cell death characterized by accumulation of free iron, reactive oxygen species generation and lipid peroxidation and is distinct from other types of regulated cell deaths such as apoptosis, necrosis and autophagy. Ferroptosis is distinct from other programmed cell deaths for its iron dependence and its significant role in tumor suppression. Therefore, harnessing ferroptosis may offer promising avenues for cancer therapy. In the present review, the different pathways that lead to ferroptosis, the genes and transcription factors involved in both iron and lipid metabolism, as well as the impact of small‑molecule alterations on the regulation of ferroptotic cell death, were discussed. Furthermore, the emergence of combination therapies with ferroptosis‑inducing molecules that overcome resistance to conventional chemotherapy, particularly in solid tumors, were highlighted.

Subsequently to the publication of the above paper, the authors have drawn to the attention of the Editorial Office that they made an error in assembling the western blot data in Fig. 3C on p. 6; namely, that the western blot data correctly selected for the P53 protein with the SW620 cell line (right-hand gels) had inadvertently also been included for the γ-H2A.X protein blots with the HCT116 cell line (left-hand gels). Upon analysing this figure further in the Editorial Office, we notified the authors of possibly overlapping α-tubulin control blots for the SW62 cell line in the same figure part, and the authors realized that one of these blots had similarly been chosen incorrectly. The revised version of Fig. 3, now showing the correct γ-H2A.X data for the HCT116 cell line and the correct α-tubulin protein blots for the SW620 cell line, is shown on the next page. The authors wish to emphasize that the corrections made to this figure do not affect the overall conclusions reported in the paper, and they are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this corrigendum. All the authors agree with the publication of this corrigendum, and also apologize to the readership for any inconvenience caused. [Oncology Reports 51: 70, 2024; DOI: 10.3892/or.2024.8729].

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].

Melanoma, a highly malignant form of skin cancer, poses significant challenges in oncology due to its aggressive nature and resistance to conventional therapies. Epigenetic modifications, especially acetylation, have emerged as critical regulators of gene expression that influence the pathogenesis and progression of melanoma. Acetylation is a novel post‑translational modification that involves the addition of an acetyl group to lysine residues both in histone and in non‑histone proteins. In the context of melanoma, acetylation has been shown to occupy a pivotal role in regulating cellular proliferation, autophagy, apoptosis and metastasis, as well as drug resistance. The identification of acetylation‑associated biomarkers and therapeutic targets in melanoma is currently an active area of research. The present review aims to elucidate the roles of acetylation modifications in melanoma, and to explore the potential of targeting these modifications for novel therapeutic interventions, with a unique perspective on the acetylation networks mediating therapy resistance.

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.

Non‑small cell lung cancer (NSCLC), accounting for >85% of LC cases, remains a therapeutic challenge due to its low 5‑year survival rate, tumor heterogeneity and drug resistance. The SRY‑related high‑mobility group‑box (SOX) family comprises transcription factors involved in the initiation and progression of NSCLC. These factors regulate epithelial‑mesenchymal transition and angiogenesis, interact with epidermal growth factor receptor/KRAS pathways to influence tumor invasion and promote chemotherapy resistance by sustaining tumor stemness. The present review aimed to summarize the expression patterns, molecular mechanisms and clinical relevance of SOX family members (such as SOX2, SOX4 and SOX9) in NSCLC, as well as their potential as diagnostic biomarkers and therapeutic targets, and the application of emerging technology in elucidating their functions. The present review aimed to provide a theoretical foundation for precision diagnostics and therapeutics to foster more effective NSCLC treatment.

Pancreatic ductal adenocarcinoma (PDAC) resistance to oxaliplatin is associated with diminished drug uptake and a poor molecular apoptotic response; however, the relative contribution of each of these modes of resistance remains unclear. Accordingly, PDAC cell lines (AsPC‑1 and BxPC‑3) and human patient‑derived organoids (hPDOs; h08 and h19) were assessed in the present study, with proliferation assays, atomic absorption spectroscopy‑based quantification of intracellular oxaliplatin, luminogenic caspase 3/7 assays, PCR array‑based transcriptomic analysis and RNA sequencing performed to scrutinize the oxaliplatin resistance phenotype. Notably, AsPC‑1 cells [half maximal inhibitory concentration (IC₅₀), 88.8±45 µM were 4.2‑fold more oxaliplatin resistant than BxPC‑3 cells (IC₅₀, 21±0.7 µM; P=0.02)]. In addition, when normalized to intracellular platinum levels, AsPC‑1 cells remained 2.5‑fold more resistant than BxPC‑3 (the fold difference was decreased by 40% from 4.2‑fold to 2.5‑fold; P=0.21). In hPDOs, resistant h19 took up oxaliplatin 22% less efficiently than sensitive h08, and the nominal resistance difference was 3.5‑fold, and it remained at 2.8‑fold after controlling for drug accumulation (the fold difference was decreased by 20% from 3.5‑fold to 2.8‑fold; P=0.34). These findings indicated that diminished drug uptake non‑significantly contributed to oxaliplatin resistance, which was in agreement with the rather minor differences in drug transporter expression levels (including ATP7A and ATP7B). Furthermore, when challenged with identical intracellular oxaliplatin levels, AsPC‑1 cells exhibited delayed caspase 3/7 activity initiation, weaker induction of pro‑apoptotic genes BBC3 (1.7‑fold vs. 5‑fold) and PMAIP (2.5‑fold vs. 6‑fold), but stronger enhancement of anti‑apoptotic Jun expression (7‑fold vs. 3‑fold) than BxPC‑3 cells. Taken together, oxaliplatin resistance in PDAC models may be highly linked to a poor apoptotic response, whereas drug uptake seems to be of minor relevance.