International journal of oncology最新文献

Subsequently to the publication of the above article, an interested reader drew to the authors' attention that certain of the tumor images shown in Fig. 7B on p. 13 had already appeared in different form in Fig. 2E in a previously published paper in the journal Frontiers in Cell and Developmental Biology written by different authors at different research institutes. Owing to the fact that the contentious data in the above article had already been published prior to its submission to International Journal of Oncology, 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. [International Journal of Oncology 60: 14, 2022; DOI: 10.3892/ijo.2022.5304].

Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that the data for the PTPRK blots shown in Fig. 1B on p. 1129 were strikingly similar to data that had already appeared in a previous publication by the same authors in the journal PLoS One. The authors have re‑examined their original data, and realize how this error occurred. The revised (and corrected) version of Fig. 1, now showing the correct data for the PTPRK blots in Fig. 1B, is shown below. The authors sincerely apologize for the error made in assembling this figure, although they confirm that this did not grossly affect either the results or the conclusions reported in this study. They also thank the Editor of International Journal of Oncology for granting them the opportunity to publish a Corrigendum, and apologize to the readership for any inconvenience caused. [International Journal of Oncology 50: 1127-1135, 2017; DOI: 10.3892/ijo.2017.3884].

Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, concerning the cell invasion assays shown in Fig. 5A on p. 1436, the 'WT' and 'pEF6' data panels contained apparently overlapping sections of data, such that these experiments were apparently derived from the same original source where the results of differently performed experiments were intended to have been portrayed. After re‑examining their original data, the authors have realized that the data panel in Fig. 5A for the 'pEF6' experiment was inadvertently selected incorrectly. The revised version of Fig. 5, showing all the correct data for Fig. 5A, is shown on the next page. 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 47: 1429‑1439, 2015; DOI: 10.3892/ijo.2015.3121].

Magnetic Resonance Imaging (MRI) relies on contrast agents to enhance image quality and diagnostic accuracy. Traditional metal‑based agents, such as gadolinium compounds, raise safety concerns due to potential toxicity and long‑term retention in the body. The present review examines recent advancements in non‑metal‑based MRI contrast agents, focusing on fluorine‑19 (19F) compounds, chemical exchange saturation transfer (CEST) agents, nitroxide radicals, and hyperpolarized carbon agents. It discussed the mechanisms by which these agents improve contrast, including their biocompatibility and ability to provide molecular and metabolic information. Key findings highlight the high specificity of19F agents due to negligible background signals, the capacity of CEST agents for molecular imaging without metals, nitroxide radicals' utility in redox‑sensitive imaging, and hyperpolarized ¹³C compounds' role in real‑time metabolic assessment. Despite challenges such as low sensitivity and technical complexities, these non‑metal‑based agents offer promising, safer alternatives with enhanced diagnostic capabilities, paving the way for more precise and personalized medical imaging.

In this review, the role of microRNA‑21 (miRNA‑21) as an oncogene in lung cancer was investigated. Studies have shown that miRNA‑21 can promote the progression of lung cancer by targeting downstream target genes, and its expression can be modulated by transcription factors, DNA methylation or competitive endogenous RNA as an upstream regulator. This review highlights that miRNA‑21 can promote the progression of lung cancer through multiple signaling pathways, with a focus on the PI3K/AKT, MEK/ERK, TGF‑β/SMAD, Hippo, NF‑κB and STAT3 signaling pathways. Mechanistically, miRNA‑21 plays an important role in the progression of lung cancer by regulating multiple biological processes, such as proliferation, invasion, metastasis, apoptosis and angiogenesis in lung cancer cells. Higher expression of miRNA‑21 is associated with chemotherapy, radiotherapy and immune resistance in lung cancer. Targeting these molecular pathways may be a novel therapeutic strategy for treating lung cancer. Additionally, miRNA‑21 can serve as a biomarker for lung cancer diagnosis, prognosis and treatment response. This review also summarized the following: i) Current methods employed to inhibit the expression of miRNA‑21 in lung cancer, including CRISPR/Cas9 technology; ii) the application of natural anticancer agents, oligonucleotides, small molecules and miRNA sponges; and iii) the nano‑delivery systems developed for miRNA‑21 inhibitors. Finally, the advancements in research on miRNA mimics and inhibitors in clinical trials, which may promote the application of miRNA‑21 in clinical trials in lung cancer, were discussed. Given that lung cancer is a considerable public health challenge, these studies provide new ways of treating patients with lung cancer.

Brain tumors are one of the most severe types of malignant tumors and glioma accounts for ~80% of malignant brain tumors. The current treatment methods for glioma are limited and patients with glioma often experience relapse following treatment, which leads to a poor prognosis for these patients. Therefore, novel therapeutic targets and methods urgently need to be explored. The present review screened studies that mainly focused on the epigenetic regulation of small guanosine triphosphate (GTP)ase in glioma. These small GTPases participate in most cellular biological processes, including differentiation, proliferation, cell migration, apoptosis, vesicle and organelle dynamics and transport, nuclear dynamics and cytoskeleton regulation. Due to the diversity and importance of the biological functions of small GTPases, an increasing number of studies have focused on them; however, the incidence of changes in the gene structure of small GTPases is considered to be low in glioma. Several studies have shown that the abnormal expression of genes encoding small GTPases is often influenced by epigenetic regulation in glioma. Epigenetic regulation is a dynamic and reversible process, which implies that the reversal of abnormal epigenetic modifications is a potential treatment strategy for glioma. These previous studies, which are summarized in the present review, not only provide new therapeutic targets and prognostic markers, but also provide information regarding the treatment of glioma. The current review may provide valuable insights for future research and promote the clinical translation of relevant research results.

Cancer‑associated fibroblasts (CAFs) represent an important component of the stromal cell population within the tumor microenvironment (TME) and are intricately linked to tumor growth, metastasis and drug resistance. In the TME, non‑coding RNAs present in exosomes act as essential mediators of intercellular communication. Exosomal RNAs derived from cancer cells activate CAFs, which in turn regulate cancer cell proliferation, invasion and drug resistance. Conversely, exosomal RNAs derived from CAFs contribute to therapeutic resistance in cancer by modulating survival signaling pathways, epithelial‑mesenchymal transition, programmed cell death, drug transporter expression levels and immune evasion. The present review examines the role and mechanisms of exosomal RNAs in CAF‑mediated cancer therapeutic resistance and offers recommendations for future research based on the underlying mechanisms of CAF‑induced drug resistance.

Triple‑negative breast cancer (TNBC) is a lethal subtype of breast cancer with a poor prognosis and limited existing treatment options. The immune checkpoint inhibitor, anti‑programmed death ligand 1 (PD‑L1), has recently emerged as a promising alternative in treating TNBC. PD‑L1 is critical in tumor immune evasion and is therefore a key target for cancer immunotherapy. Although anti‑PD‑L1 therapy is effective in breast cancer based on clinical trials, the relationship between PD‑L1 expression levels and treatment response remains unclear. To investigate this, a 4T1 breast cancer cell line that stably overexpressed PD‑L1 was established and was used to create a tumor model in mice. Mice were treated with anti‑PD‑L1 antibodies, and tumor growth was compared between the control and treated groups. PD‑L1 overexpressing tumors did not exhibit an antitumor response to anti‑PD‑L1 therapy compared with the control tumors. Additionally, immune cell infiltration and activation were significantly altered, as shown by immunohistochemical staining and bulk RNA sequencing. In PD‑L1‑overexpressing tumors that did not respond to treatment, immune cell markers and antitumor immune pathways were downregulated. These results demonstrated that excessive PD‑L1 expression creates an immunosuppressive tumor microenvironment, which impairs the efficacy of anti‑PD‑L1 therapy. The present study suggests that excessive PD‑L1 expression reduces the effectiveness of antitumor immunotherapy, and that PD‑L 1 expression levels are essential in predicting the response to antitumor immunotherapy.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell migration assay experiments shown in Fig. 1C and 3C, three sets of data panels were found to contain overlapping sections of data (including four panels across the figure parts that contained the same overlapping data). A further pair of overlapping data panels were identified for the immunofluorescence experiments shown in Fig. 5. Upon receiving notification of this issue, the authors requested a corrigendum and submitted corrected versions of Figs. 1, 3 and 5. However, upon performing an independent analysis of the data in this paper in the Editorial Office, it was also noted that certain of the data in these figures had appeared subsequently in a pair of more recent publications by the same research group, and moreover, one of these images had been incorporated into one of the three revised figures submitted for the corrigendum. Owing to the large number of duplications of data identified in the published paper, and the apparent mislabelling of the authors' own data files, 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. After contacting the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 45: 1123-1132, 2014; DOI: 10.3892/ijo.2014.2527].

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the different cell invasion and migration assay experiments shown in Fig. 5 on p. 238, as many as four pairs of overlapping data panels were identified, such that these data panels had all apparently been derived from the same original source(s); in addition, a further pair of overlapping data panels was identified comparing between Fig. 5 and the cell migration and invasion assay experiments shown in Fig. 7. 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 satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 47: 231‑243, 2015; DOI: 10.3892/ijo.2015.2981].