Oncology reports最新文献

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 Oncology Reports 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].

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.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the GAPDH and MEF21 protein bands shown in the western blots in Fig. 2C on p. 2608 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published, or were under consideration for publication at the same time, some of which have subsequently been retracted. Upon conducting an independent evaluation of the data in the Editorial Office, it emerged that the western blots shown in Fig. 1B in this paper had similarly appeared in a number of unrelated articles.In view of the fact that the abovementioned data in Figs. 1B and 2C had already apparently been published previously, the Editor of Oncology Reports 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. [Oncology Reports 33: 2606‑2612, 2015; DOI: 10.3892/or.2015.3861].

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 Oncology Reports 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].

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.

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.

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 Molecular Medicine Reports 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].

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.

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 vivo. 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.

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.