International journal of oncology最新文献

Gastric cancer (GC) is a major global health burden, ranking fifth in incidence and third in cancer‑related mortality. By 2040, there are expected to be ~1.8 million new cases and 1.3 million fatalities associated with GC. Spasmolytic polypeptide‑expressing metaplasia (SPEM) is a central component of gastric precancerous lesions, which remodels the gastric mucosa in response to injury through a lineage of mucus‑secreting cells. Interleukins (ILs) are the communication means for innate and adaptive immune cells as well as non‑immune cells and tissues. Their complex network regulation contributes to the development of SPEM and is a key driver in the transformation of SPEM to GC. The present review systematically described the IL‑related mechanisms underlying the formation and progression of SPEM and categorizes the roles of different ILs by family. In addition, the molecular association between IL dynamics and SPEM following Helicobacter pylori infection is explored, and various SPEM experimental model characteristics and IL‑based therapeutic strategy advances and limitations are discussed. The clinical translation of IL‑targeted therapies is limited, but the development of therapies that target pathogenesis specifically and the enhancement of IL therapy combinations with other therapeutic options may improve efficacy and reduce side effects. Increased understanding of the causes of SPEM and the mechanisms underlying GC may open up new avenues for early detection and targeted therapy.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the bioluminescence and fluorescence images of the mouse shown in Fig. 2C and E respectively, the images/positioning of the mouse appeared to be unexpectedly similar, and the authors were asked to confirm whether the images were captured at the same time, but separate results were obtained for the luminescence and fluorescence readings. Similarly, in Fig. 3A, the same mouse image (re. its appearance and positioning) appeared to be shown for the 5a‑D‑Luc cell line on Days 14 and 28, albeit with different bioluminescence. Finally, upon analyzing the data independently in the Editorial Office, it came to light that, for the phase contrast images of the MDA‑MD‑231 and 5a‑D‑Luc cell lines shown in Fig. 1A, these appeared to be the same image, but with different lighting intensities and with the 5a‑D‑Luc image rotated through 90˚. The authors were contacted by the Editorial Office to offer an explanation for these possible anomalies in the presentation of the data in this paper, although 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 conitnues to investigate this matter further. [International Journal of Oncology 48: 525‑532, 2016; DOI: 10.3892/ijo.2015.3300].

Treatment of urothelial carcinoma (UC), particularly in metastatic or cisplatin‑ineligible patients, remains challenging because of limited durable responses to conventional chemotherapy and immune checkpoint inhibitors. Recent advances in targeted therapies, including FGFR inhibitors (for example, erdafitinib) and antibody‑drug conjugates (ADCs) targeting Nectin‑4 (enfortumab vedotin) and HER2 (disitamab vedotin), have reshaped treatment paradigms. FGFR3 alterations, which are present in 20‑40% of patients with advanced UC, predict sensitivity to FGFR tyrosine kinase inhibitors, whereas ADCs demonstrate efficacy across biomarker‑selected and unselected populations. However, clinical implementation is complicated by resistance mechanisms, such as kinase switching, phenotypic plasticity and tumor microenvironment interactions, as well as biomarker heterogeneity. The present review synthesizes current evidence on molecularly guided therapies, contrasts resistance mechanisms between FGFR inhibitors and ADCs, and evaluates strategies to overcome therapeutic limitations. By integrating translational insights and emerging preclinical data, it was aimed to provide a roadmap for optimizing biomarker‑driven approaches, novel combinations and next‑generation agents for the treatment of UC.

Prostate cancer remains one of the most prevalent malignancies and a major cause of cancer‑related mortality among men worldwide. Despite widespread use of prostate‑specific antigen testing, current diagnostic approaches suffer from low specificity and limited ability to distinguish between indolent and aggressive disease, resulting in overdiagnosis and overtreatment. Advances in molecular biology, genomics and metabolomics have led to the identification of novel biomarkers that have potential for improving the precision of prostate cancer diagnosis, prognosis and therapy. The present review provides a comprehensive overview of emerging prostate cancer biomarkers, including genetic (such as BRCA1/2, HOXB13 and PTEN), RNA‑based (such as PCA3 and miRNAs), metabolic (such as citric acid and polyamines) and methylation markers (such as GSTP1, APC and RASSF1A). These biomarkers not only enhance diagnostic accuracy but also facilitate risk stratification, prediction of therapeutic response and real‑time disease monitoring through liquid biopsy technologies. Moreover, integrating multi‑omics data with artificial intelligence and machine learning may further improve early detection and personalized treatment strategies. Overall, the development and clinical implementation of these biomarkers represent a transformative step toward precision medicine in prostate cancer, enabling earlier diagnosis, optimized therapy selection and improved patient outcomes.

Oncolytic virotherapy has emerged as a significant advancement in cancer treatment. However, the efficacy of monotherapies is limited by tumor heterogeneity, highlighting the need for combination strategies to overcome therapeutic limitations. This study provides a review of the molecular mechanisms, preclinical advancements and clinical outcomes associated with oncolytic virus (OV)‑targeted drug combinations over the past two decades, elaborating on the interaction mechanisms through which molecular targeted drugs and oncolytic viruses enhance antitumor effects. Additionally, the progress in translating OV‑based combination therapies for solid tumors into clinical practice is outlined and innovative strategies are proposed for developing novel therapeutic frameworks.

The present study focused on the role of coiled‑coil domain‑containing protein 137 (CCDC137), an RNA‑binding and epigenetic protein with high expression and poor prognosis in various types of cancer. Bioinformatics analysis, cellular experiments and animal models investigated the functions of CCDC137 in RNA post‑transcriptional regulation, epigenetic modification and the tumor microenvironment. The results showed that CCDC137 can bind specific mRNAs to affect physiological processes such as the cell cycle, participate in epigenetic regulation such as DNA methylation and histone modification and influence tumor immune escape by affecting the functions of tumor‑associated macrophages. Based on the multidimensional regulatory functions of CCDC137, it is expected to become a new target for cancer diagnosis and treatment and provide a theoretical basis for precision cancer therapy.

Cancer stem cells (CSCs), a small subpopulation of cancer cells that exhibit stem‑like properties, possess the ability to differentiate and self‑renew. These capabilities enable CSCs to act as tumor‑initiating cells, driving tumorigenesis and proliferation, leading to major clinical challenges. Specifically, CSCs play a crucial role in metastasis, recurrence and drug resistance, thereby leading to complications in therapeutic responses. The plasticity of CSCs leads to heterogeneity, allowing them to adopt diverse phenotypes in response to intrinsic genetic factors or extrinsic environmental cues. This adaptability may serve as a mechanism for CSCs to thrive in the tumor microenvironment (TME) and promote tumor progression. The present article aimed to review the multifaceted nature of CSCs, examining their functional diversity, biomarkers and interactions with the TME. Through elucidating the mechanisms that underlie this heterogeneity, researchers aim to develop targeted therapeutic interventions against CSCs, thereby enhancing the efficacy of cancer treatments and improving patient outcomes.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the tumor images shown in Fig. 4A on p. 1180 were unexpectedly similar, albeit the images appeared to have been horizontally stretched where they reappeared in the figure, under situations where different experiments were intended to have been shown. Owing to the anomalies identified in this figure, the Editor of International Journal of Oncology 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 45: 1175‑1183, 2014; DOI: 10.3892/ijo.2014.2498].

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the Bcl‑2 protein bands shown for the HCC827 cell line in the western blots in Fig. 3A on p. 342 were unexpectedly similar to the Akt protein bands shown for the A549 cell line in Fig. 3B. In addition, the Bcl‑2 protein bands shown for the H358 and HCC827 cell lines (the left‑hand and middle gels) possibly contained a pair of mutually overlapping protein bands, and the β‑actin control bands featured in the left‑hand and middle lanes of Fig. 3A for the H358 and HCC827 cell lines, and the β‑actin control bands featured in the middle and right‑hand lanes for the H358 and HCC827 cell lines in Fig. 1C on p. 340, were similarly more similar than might have been expected. The authors were contacted by the Editorial Office to offer an explanation for this possible anomaly in the presentation of the data in this paper, although 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. [International Journal of Oncology 35: 337‑345, 2009; DOI: 10.3892/ijo_00000345].

Radiotherapy is an important treatment for tumors; however, some patients exhibit poor sensitivity to radiation, leading to unsatisfactory outcomes. mTOR regulates critical processes such as cell proliferation, autophagy and DNA repair, serving a central role in tumor biology. Moreover, mTOR inhibitors have shown potential to enhance radiotherapy effectiveness and address radiation resistance. Although drug resistance and side effects limit their clinical use, combining therapies and optimizing treatment plans could improve results. The present review summarizes how mTOR signaling contributes to radiation resistance in lung cancer, as well as the underlying molecular mechanisms. Understanding these pathways may aid the development of new combination therapies to improve treatment options for patients with lung cancer.