International journal of oncology最新文献

Following the publication of the above article, the authors drew to the Editor's attention that, for the fluorescence microscopy experiments shown in Fig. 7 on p. 2506, they had inadvertently included the same data to show the results for the 'Control' and 'CCL19 + CCR7 mAb' experiments for E‑cadherin (top row, first and third images from the left). The Editorial Office subsequently conducted an independent assessment of the data in this paper and, regarding the scratch‑wound assay experiments shown in Fig. 5 also on p. 2506, two pairs of the images contained overlapping sections, 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 their original data, the authors have realized that Fig. 5 was also presented incorrectly, and the revised versions of Fig. 5, now containing the correct images for the 'CCL19+PD98059 0 h', 'CCL19+SP600125 0 h' and 'CCL19+SP600125 24 h' experiments, and of Fig. 7, now showing the correct data for the E‑cadherin 'Control' experiment, are shown on the next page. The authors wish to state that these errors did not affect the overall conclusions reported in the study. The authors are grateful to the Editor of International Journal of Oncology for allowing them this opportunity to publish a Corrigendum, and all the authors agree with its publication. Furthermore, the authors apologize to the readership for any inconvenience caused. [International Journal of Oncology 45: 2502‑2510, 2014; DOI: 10.3892/ijo.2014.2674].

Immune checkpoint blockade therapy has revolutionized cancer treatment, yet its clinical efficacy remains limited to a subset of patients with specific tumor types. The present review provides a comprehensive analysis of T cell‑mediated antitumor immunity from both local and systemic perspectives, with particular emphasis on CD8⁺ T cells as primary effectors. The review discusses how the complex trafficking between the tumor microenvironment (TME), surrounding lymphoid tissues and peripheral circulation creates multiple opportunities for tumors to evade immune surveillance. Within the TME, T‑cell exclusion mechanisms, antigen specificity and the spectrum of T‑cell exhaustion states, from progenitor exhausted T cells to terminally exhausted T‑cell phenotypes, are reviewed. Beyond the local TME, the crucial roles of tumor‑draining lymph nodes and tertiary lymphoid structures in maintaining sustainable antitumor immunity, as well as the significance of circulating T cells as both biomarkers and therapeutic targets, are analyzed. This systemic perspective provides insights into the dynamic nature of antitumor immunity and suggests potential strategies for next‑generation immunotherapies, including combination approaches targeting multiple immune compartments to achieve optimal therapeutic outcomes.

Sesquiterpenoids are widely distributed in plants, animals, marine organisms and microorganisms, particularly in Asteraceae plants, and they exhibit various biological activities, including anti‑tumor, anti‑bacterial, anti‑inflammatory, antiviral and antioxidant properties. They also have the effects of protecting the liver, protecting the nerves, preventing and treating diabetes and improving immunosuppressive function. Hepatocellular carcinoma (HCC) is the main type of primary liver cancer and the third leading cause of cancer‑related death worldwide. There is accumulating evidence that HCC is an increasingly serious threat to human health and the incidence of primary liver cancer is also still increasing. For the present review, literature on sesquiterpenoids in the treatment of liver cancer from 2003 to 2024 was searched through electronic databases. A total of 46 sesquiterpenoids were identified for HCC treatment. It was found that sesquiterpenoids play a therapeutic role in HCC by inhibiting proliferation, inducing apoptosis, inhibiting invasion and metastasis of HCC cells, regulating the body's immune function and decreasing the resistance of tumor cells. Sesquiterpenoids are promising drugs, which may create more opportunities for the treatment of liver cancer. However, research on how sesquiterpenoids act on HCC is not systematic and most reports are also limited to mixtures, while there is only a small number of reports of new sesquiterpene monomers for treating HCC. Therefore, it is necessary to further discover new components and study their biological activities, and to gradually conduct in‑depth in vivo studies and clinical application in the future. The present study reviewed the research progress of sesquiterpene‑rich natural products in the treatment of HCC in the past two decades.

Cancer stem cells (CSCs) are a distinct subpopulation of cells within tumors, characterized by their ability to self‑renew, differentiate and promote tumorigenesis. CSCs have critical roles in the initiation, progression and therapeutic resistance of digestive tract tumors, including in esophageal, gastric, colorectal and pancreatic cancer. The present review comprehensively explores the biology of CSCs, their interactions with the tumor microenvironment and their clinical relevance in predicting patient prognosis and guiding treatment strategies. The emerging therapeutic approaches that target CSCs, including pathway inhibitors, monoclonal antibodies and combination therapies, are also discussed, highlighting the potential of these strategies to improve patient outcomes in digestive tract cancer types. Additionally, future research directions and challenges in developing effective CSC‑targeted therapies are addressed, emphasizing the need for innovative strategies to overcome treatment resistance and increase therapeutic efficacy.

Following the publication of the above article, an interested reader drew to the authors' attention that, for the fluorescence microscopic images shown in Fig. 4A on p. 425, the data shown for the 'Huh7 / pcDNA3.1‑MEG3' experiment appeared to repeat some of the data shown in the 'HepG2 / pcDNA3.1‑MEG3' experiment, albeit at a different magnification. Upon examining their original data, the authors realized that they had inadvertently assembled the data in this figure incorrectly. The revised version of Fig. 4, now showing the correct images for the Control and pcDNA3.1‑MEG3 experiments for the Huh7 cell line, is shown on the next page. The authors wish to state that these errors did not affect the overall conclusions reported in the study. The authors are grateful to the Editor of International Journal of Oncology for allowing them this opportunity to publish a Corrigendum, and all the authors agree with its publication. Furthermore, the authors apologize to the readership for any inconvenience caused.  [International Journal of Oncology 48: 421‑429, 2016; DOI: 10.3892/ijo.2015.3248].

Gliomas are the most common primary brain tumors, and exhibit highly heterogeneous and aggressive biological behaviors. Metabolic reprogramming is a hallmark of gliomas, and lactate accumulation serves a critical role in tumor progression. In addition to its traditional role as a metabolic byproduct, lactate has been recognized as a signaling molecule that modifies proteins through lactylation, which is a novel post‑translational modification. Lactate‑induced lactylation of histone and non‑histone proteins is emerging as a key epigenetic and metabolic regulator that influences glioma development, immune evasion, angiogenesis and therapeutic resistance. The present review provides mechanistic insights into protein lactylation, its role in glioma progression and its potential therapeutic implications. Targeting lactate metabolism and lactylation‑modifying enzymes holds promise for improving glioma treatment outcomes.

Oxaliplatin (OXA) is a first‑line chemotherapy agent for hepatocellular carcinoma (HCC); however, its application is hindered by low therapeutic sensitivity and severe adverse effects. Acteoside (ACT) has both antitumor and hepatoprotective properties. Therefore, the present study investigated the mechanisms underlying the synergistic and toxicity‑reducing effects of ACT as an adjuvant to OXA in HCC therapy. Liver cancer cell lines and a xenograft mouse model were treated with ACT and/or OXA. In vitro Cell Counting kit‑8, Transwell invasive assay, wound healing assay, cell cycle and apoptosis detection assays assessed cell viability, migration, invasion, cell cycle progression and apoptosis to evaluate the synergistic effects of the combination therapy. In vivo studies examined tumor growth, cell proliferation, survival time and blood biochemical indices. The effects of ACT on OXA‑induced toxicity were also evaluated. Transcriptomics and metabolomics analyses were integrated to elucidate the mechanisms by which ACT enhances OXA efficacy and mitigates its toxicities. The results revealed that ACT synergized with OXA to inhibit HCC progression both in vivo and in vitro. ACT significantly alleviated OXA‑induced toxicity, particularly neurotoxicity. Mechanistically, phosphatidylinositol signaling system‑associated genes/proteins exerted important roles in the anti‑HCC effects of ACT. Western blotting revealed that ACT‑induced upregulation of INPP4B inhibited the PI3K/AKT signaling pathway, which may underlie its ability to enhance the therapeutic efficacy of OXA and reduce its toxic effects. In conclusion, ACT enhanced efficacy and reduced the toxicity of OXA in the treatment of HCC, potentially via the regulation of INPP4B to inhibit the PI3K/AKT signaling pathway.

Triple‑negative breast cancer (TNBC) is a highly aggressive and heterogeneous subtype of BC characterized by the absence of estrogen, progesterone and human EGFR2 receptors. This lack of receptors renders it unresponsive to standard targeted therapies. Despite advances made in understanding the molecular landscape of TNBC, its poor prognosis and high recurrence rates underscore the urgent need for innovative therapeutic approaches. This review explores the effects of key prognostic markers, such as Ki‑67, programmed cell death ligand 1, BRCA1/2 mutations, E‑cadherin loss and EGFR alterations. It also examines critical pathways, including the PI3K/AKT/mTOR and mutant p53 pathways, which are prerequisites for TNBC progression and therapy resistance, and discusses the therapeutic potential of directly targeting these key molecules and their associated signaling pathways. In addition, recent advances in targeted therapies were highlighted, such as immune checkpoint inhibitors, and the statuses of emerging strategies were presented, such as chimeric antigen receptor‑T cell therapy and small inhibitory RNA‑based treatments. Given the molecular heterogeneity of TNBC, the importance of precision medicine was also discussed and it was emphasized that this approach is becoming an increasingly critical aspect of personalized treatment strategies. Resistance to existing therapies presents a major challenge to the effective treatment of TNBC, and thus, the development of future therapeutic strategies requires technical innovations. By integrating these insights, this review aims to provide a comprehensive overview of current and future means of improving TNBC outcomes.

Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, in Fig. 3 on p. 1356 showing the results of cellular apoptosis experiments, the 'Doxy 5 µg/ml' and 'Doxy 10 µg/ml' data panels appeared to contain overlapping data, such that these images were apparently derived from the same original source where the results of differently performed experiments were intended to have been shown. In addition, in Fig. 4A on p. 1357, showing the results of TUNEL assay experiments, the 'Doxy 10 µg/ml' and '5‑FU 25 µg/ml' data panels contained overlapping sections, similarly suggesting that these data had been derived from the same original source. The authors were able to consult their original data, and recognized how these errors occurred. The corrected versions of Figs. 3 and 4, now showing the correct data for the 'Doxy 5 µg/ml' experiment in Fig. 3 and the '5‑FU 25 µg/ml' experiment in Fig. 4A, are shown below and 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 International Journal of Oncology for allowing them the opportunity to publish this Corrigendum. Note that the errors that were made in compiling this pair of figures 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. [International Journal of Oncology 48: 1353‑1360, 2016; DOI: 10.3892/ijo.2016.3375].

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, in Fig. 1A and Fig. 3A and B showing the results of Transwell invasion and migration experiments, the majority of the data panels were identified as having overlapping sections, such that the affected data panels, which were intended to show the results of differently performed experiments, had all apparently been derived from the same original sources. Owing to the large number of duplications of data that have been identified in this paper, the Editor of International Journal of Oncology has decided that it 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. [International Journal of Oncology 47: 641‑649, 2015; DOI: 10.3892/ijo.2015.3034].