Oncology reports最新文献

Mebendazole (Mbz), a well‑known anthelminthic drug, has demonstrated anticancer properties in tumor models and patients, and is thus under consideration for repositioning into an anticancer drug. Mbz is directly cytotoxic in cell lines by various mechanisms and acts indirectly via immunomodulation. In the present study, the anticancer effects of Mbz, alone and in combination with cytotoxic drugs, were further characterized using primary cultures of patient tumor cells ex vivo and the murine colon cancer cell line, CT26, in vitro and in vivo. Patient‑derived tumor cells from acute myeloid leukemia (AML) and ovarian, colorectal and renal cancer were exposed to Mbz alone and, for solid tumors and the CT26 cell line, in combination with irinotecan, cisplatin or gemcitabine (patient cells only). Cytotoxicity was assessed using the fluorometric microculture cytotoxicity assay. In vivo, the antitumor effects of Mbz and irinotecan, alone and in combination, were evaluated in the BALB/c CT26 colon cancer mouse model by tumor growth measurements and flow cytometric analysis of tumor immune cell infiltration. In the patient cell samples, Mbz showed modest single‑agent cytotoxicity, with the AML samples being the most sensitive, and displayed enhanced effects when combined with cytotoxic drugs, particularly irinotecan. CT26 cells showed modest dose‑independent sensitivity to Mbz, which enhanced the effect of both cisplatin and irinotecan. In vivo, Mbz and irinotecan both inhibited tumor growth, but the combination did not significantly outperform Mbz alone. Flow cytometry of the resected mouse tumors indicated that Mbz promoted macrophage polarization from the M2 to M1 phenotype, suggesting that immune modulation may contribute to its anticancer effect. Mbz has features making it a candidate for repositioning into an anticancer drug and part of its effect may be mediated by macrophage modulation.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, concerning the  flow cytometric plots featured in Fig. 3A‑C on p. 1215, certain groups of data points appeared more similar to each other than might be expected. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. Therefore, 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 Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 1213‑1221, 2016; DOI: 10.3892/or.2015.4443].

Breast cancer (BC) ranks among the most prevalent malignant tumors in female patients. It represents a longstanding challenge to medical professionals in terms of diagnosis and treatment. Exploring BC pathogenesis offers insight into its complexity and facilitates the exploration of more effective treatment strategies. The present review aimed to describe the involvement of the immune system, inflammatory response and regulated cell death in BC development, offering avenues for novel therapeutic strategies against BC. Identifying novel treatment methods is key for enhancing the prognosis of patients with BC.

Following the publication of the above article, the authors drew to the Editor's attention that certain of the data in Fig. 6 on p. 74 had been assembled incorrectly. Specifically, the data panels showing the results of the SW1990/oVV/H&E and the SW1990/GEM/oVV/H&E experiments, and the SW1990/Gemcitabine/IHC‑Smac and the SW1990/GEM/oVV/IHC‑Smac experiments, respectively, contained overlapping sections, such that the data, which were intended to show the results of differently performed experiments, had been derived from the same original sources. Furthermore, upon performing an independent analysis of the data in the Editorial Office, it was noted that the data panels selected for the SW1990/oVV‑Smac/TUNEL and the SW1990/Gemcitabine&oVV‑Smac/TUNEL experiments also contained overlapping sections, and concerning the western blot data shown in Fig. 3B on p. 71, the Survivin protein bands were strikingly similar to data which had appeared in an earlier paper featuring some of the same authors in the journal Scientific Reports. After having re‑examined these figures, the authors realized that these additional cases of data duplication/re‑use were also in need of correction. The revised versions of Figs. 3 and 6, now showing the correct data for the SW1990/GEM/oVV/H&E, SW1990/GEM/oVV/IHC‑Smac and SW1990/oVV‑Smac/TUNEL experiments in Fig. 3, and the correct Survivin western blot data in Fig. 6, are shown on the next page. The authors wish to emphasize that the errors made in terms of the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for granting them this opportunity to publish a Corrigendum, and apologize to both the Editor and the readership for any inconvenience caused. [Oncology Reports 41: 67‑76, 2019; DOI: 10.3892/or.2018.6817].

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the 'Mock' and 'mimic‑18a NC' data panels shown in Fig. 5A for the SiHa flow cytometric (FCM) experiments were remarkably similar in appearance, even though their gated percentages were reported differently. Upon performing an independent analysis of the data in the Editorial Office, it came to light that various of the data quadrants shown in this figure were strikingly similar to FCM data in articles written by different authors at different research institutes that were published subsequently in other journals, one of which has been retracted on account of data re‑use issues; in addition, data were apparently duplicated in Fig. 10A, where the same data had been used to show the results of differently performed experiments. Given the nature of the contentious issues repported above, 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 33: 2853‑2862, 2015; DOI: 10.3892/or.2015.3929].

Cancer cells play a pivotal role in immune evasion by activating the programmed cell death protein 1 (PD‑1)/PD‑ligand (L)1 signaling pathway or immune cells within the tumor microenvironment. The ubiquitin‑proteasome system (UPS), the primary pathway for intracellular protein degradation, has been increasingly implicated in mediating tumor immune escape and resistance to anti‑PD‑1/PD‑L1 therapy. Targeting the UPS has demonstrated significant potential in improving the efficacy of tumor immunotherapy. Therefore, a deeper understanding of the molecular mechanisms by which UPS contributes to tumor resistance against PD‑1/PD‑L1 blockade, along with the optimization of UPS‑targeted small‑molecule drug design, holds scientific and clinical significance. In the present review, the role of UPS in tumor immune evasion through the regulation of PD‑1/PD‑L1 ubiquitination was discussed and potential therapeutic agents that may enhance the effectiveness of anti‑PD‑1/PD‑L1 treatment are summarized. These insights provide a theoretical foundation for advancing cancer immunotherapy and developing novel combination strategies.

Chronic myeloid leukemia (CML) is a hematological malignancy driven by diverse genetic aberrations, with the Philadelphia chromosome and its resultant BCR‑ABL1 fusion gene constituting key pathogenic drivers. Atypical BCR‑ABL1 fusion transcripts have distinctive structural and functional properties. Structural divergence in these variants leads to functional alterations of encoded oncoproteins, potentially influencing disease progression and therapeutic responsiveness. Conventional diagnostic modalities, including reverse transcription‑PCR and fluorescence in situ hybridization, may fail to detect rare variants, necessitating complementary high‑sensitivity techniques such as next‑generation sequencing). Tyrosine kinase inhibitors (TKIs), including imatinib and dasatinib, remain cornerstone treatments; however, marked inter‑variant heterogeneity in TKI responsiveness is observed: Patients harboring e13a3/e14a3 transcripts generally show favorable prognoses, while those with e1a3/e6a2 variants demonstrate an increased risk of relapse and/or TKI resistance, often requiring multimodal strategies combining chemotherapy or allogeneic hematopoietic stem cell transplantation. Although Chimeric Antigen Receptor)‑T cell therapy has shown promise in treating (Philadelphia chromosome‑positive B‑cell Acute Lymphoblastic Leukemia, its application in CML, particularly in variants such as e1a3 or e6a2, is not currently recommended as a first‑line treatment. Despite advances in elucidating the clinical implications of fusion gene heterogeneity in leukemogenesis, the prognostic value of atypical BCR‑ABL1 isoforms requires further validation through multicenter studies with extended cohorts. This review aimed to summarize cases of atypical fusion genes in CML, with analysis of clinical characteristics, therapeutic interventions, and prognostic outcomes, to provide clinicians with enhanced reference material for improved patient management.

Thyroid cancer is the most common malignant endocrine tumor. Differentiated thyroid cancer (DTC) accounts for 95% of thyroid cancer cases. The primary treatment for intermediate‑ and high‑risk DTC is total thyroidectomy. Postoperatively, serum thyroglobulin (Tg) and anti‑Tg antibody (Tg/Ab) levels are monitored to detect residual, recurrent or metastatic disease. Radioactive iodine (¹³¹I) therapy is administered orally when Tg and Tg/Ab levels exceed standard levels. Recombinant human thyroid‑stimulating hormone (rhTSH) administration methods that do not require thyroid hormone withdrawal treatment and hospitalization have been recommended. However, serum Tg levels, a biomarker of thyroid tissue ablation, are often disturbed by Tg/Ab interference, which is observed in one‑quarter of patients with DTC. The present study aimed to elucidate the molecular mechanisms underlying metabolic changes in patients with DTC treated with ¹³¹I, and to identify Tg/Ab‑independent biomarker candidates using the TPC‑1 cell model. Blood serum samples were collected from patients with DTC before and after administration of ¹³¹I, which was performed following stimulation with rhTSH. Intra‑individual variations in Tg and Tg/Ab levels were observed in the same patients before and after ¹³¹I administration. Serum metabolomic analysis showed elevated levels of branched‑chain amino acid (BCAA), including valine, leucine and isoleucine, in all 3 patients, who exhibited favorable clinical outcomes. Although the number of cases was limited, this may suggest a possible association between BCAA levels and treatment response. Additionally, while overall boronophenylalanine uptake decreased in the total cell population after ionizing radiation exposure, the surviving viable TPC‑1 cells exhibited relatively increased amino acid uptake, assessed using boronophenylalanine as a leucine analog, which corresponded to the findings presented in the cell‑based experiments. Higher expression levels of the CD98 cell surface antigen were observed in irradiated TPC‑1 cells compared with non‑irradiated controls, which may contribute to increased uptake of BCAAs. However, the mRNA expression levels of L‑type amino acid transporter type 1 (LAT1), L‑type amino acid transporter type 2 and CD98hc did not change upon exposure to IR. These results indicated that the increased BCAA uptake in IR‑exposed DTC cells was a transient response likely mediated by LAT1/CD98hc at the cell surface, as suggested by flow cytometry analysis, despite no corresponding increase in LAT1 mRNA expression.

Although our understanding of the molecular and cellular factors involved in the development and growth of glioma has increased, prognosis remains dismal in most patients. The emerging field of cancer neuroscience has revealed the intricate functional interplay between glioma and the cellular architecture of the brain, especially neural circuits. In recent years, studies have revealed that glioma cells integrate and remodel multicellular neural circuits. Neural circuits have thus emerged as critical regulators of glioma from initiation to malignant growth. In the present review, an updated framework was provided for understanding the construction of neuron‑glioma networks and the mechanisms by which neurons regulate the malignant phenotype of glioma. Readers will also obtain insights into the construction of glioma‑glioma networks formed by tumor microtubes. Furthermore, the present review reveals the complex interconnectivity among the nervous system, immune system and glioma that promotes tumor growth. Finally, some potential areas of clinical translation and new research directions were highlighted.

Due to the persistently high global incidence and mortality rates of cancer, developing novel therapeutic strategies is imperative. The replication factor C (RFC) family, a critical subset of DNA replication and repair, serves multifaceted roles in tumor progression. Despite its widely recognized importance, the pleiotropic mechanisms of the RFC family lack systematic illustration, particularly regarding each member specific contributions to cancer hallmarks. In the present review, mRNA expression of each RFC family member in pan‑cancer was profiled and the associations between their expression levels and tumor types evaluated. In addition, the effect of RFC expression on patients' survival across malignancies is assessed. Furthermore, the present review summarized current research on RFC family members in various malignancies with particular emphasis on the RFC‑like complexes, highlighting key findings and advancements in understanding their role in tumor biology. The signaling pathways associated with RFC family members are discussed and the molecular mechanisms elucidated. Finally, the clinical importance of RFC family members including prognosis, potential inhibitors and combination treatments are also discussed. The present review aimed to provide innovative perspectives for developing combinatorial molecular targeted therapies in the future.