Oncology reports最新文献

Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations are among the most frequent oncogenic drivers in cancer, particularly in non‑small cell lung cancer (NSCLC). KRAS was previously considered an 'undruggable' target due to the protein's smooth molecular surface and the absence of obvious drug binding sites. However, the development of selective KRAS G12C inhibitors, such as sotorasib and adagrasib, together with progress in immunotherapy, have demonstrated potential clinical activity. Further understanding of the complex signaling networks driven by KRAS has revealed new opportunities to target this pathway directly or through rational combination strategies. The present review explored KRAS‑targeted therapies and immunotherapies, including limitations, resistance mechanisms and the efficacy of combination regimens. Although there has been notable progress, concerns regarding optimal therapy combinations, resistance management and early treatment strategies remain. The present review demonstrated the need for continued research to address these challenges and improve outcomes for patients with KRAS‑mutated NSCLC.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data shown in Fig. 3C, the immunohistochemical data shown in Fig. 4B and the western blots in Fig. 5B had already been submitted to, or were published in, articles in other journals that featured some of the same authors; moreover, some of these data subsequently appeared in different articles in other journals that were not connected with either this research group or this research topic. Upon investigating these issues further in the Editorial Office, it was noted that, concerning Figs. 3‑5 and as far as those papers sharing some of the same authors was concerned, the cases of data sharing weren't necessarily as simple as the data merely being duplicated. Given the sharing of these contentious data across a number of different journals, 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 32: 1571‑1577, 2024; DOI: 10.3892/or.2014.3386].

Colorectal cancer (CRC) is the third most common cancer globally and the second leading cause of cancer‑related mortalities. Surgery‑centered multimodal therapy remains the cornerstone of care, yet outcomes are poor in advanced or drug‑resistant disease. The tumor immune microenvironment (TIME), a network of immune cells, cytokines and stromal elements, shapes antitumor immunity and can either restrain or encourage tumor growth. Specific immune cells within the TIME influence CRC biology, while immune‑checkpoint blockade has delivered notable benefits, especially in microsatellite instability‑high tumors. The present review discusses the principal immune cell populations in the CRC TIME, outlines their mechanisms of action and discusses emerging cell‑based immunotherapies that may guide future precision treatment.

Hepatocellular carcinoma (HCC) represents the most common form of primary liver cancer and is characterized by a significant rate of recurrence. However, there is still a lack of effective therapeutic methods. Accumulating evidence has highlighted the importance of homeobox containing 1 (HMBOX1) in tumorigenesis. However, the relationship between HMBOX1 expression and HCC remains unclear. In the present study, through the analysis of public databases and staining analysis of tissue microarrays, it was found that compared with normal tissues, HMBOX1 was significantly downregulated in tumor tissues. Furthermore, through analyses such as Cell Counting Kit‑8 assay, wound healing assay and colony formation, it was found that overexpression of HMBOX1 could inhibit cell proliferation and migration, while silencing of HMBOX1 promoted tumor biological characteristics in HCC cell lines. The molecular biological mechanism was explored by using proteomics combined with bioinformatics analysis and western blotting. Mechanistically, AKT1 was identified as a downstream effector of HMBOX1, and protein tyrosine phosphatase non‑receptor type 1 (PTPN1) signaling might mediate the regulation of AKT1 by HMBOX1. In vivo tumor‑bearing experiments also verified the function of the HMBOX1/PTPN1/AKT1 pathway in HCC development. Taken together, the present findings revealed a new HMBOX1/PTPN1/AKT1 axis that inhibits tumor progression and provides new candidate therapy targets for HCC.

Bone sarcomas remain lethal despite multimodal therapy, primarily because the mineralized, immunosuppressive tumor microenvironment (TME) promotes chemo‑ and immune‑resistance. Integrating single‑cell and spatial omics across osteosarcoma, Ewing sarcoma and chondrosarcoma delineates subtype‑specific TME archetypes dominated by M2 macrophages, exhausted T cells and a stiff extracellular matrix. Mechanistic dissection reveals tractable vulnerabilities, myeloid reprogramming, extracellular matrix modulation and metabolic and epigenetic checkpoints, that can be targeted with bone‑selective delivery systems and biomarker‑driven combination trials to convert therapeutic failure into durable remission. Therefore, the aim of the present review is to synthesize the latest single‑cell, spatial and functional data to map bone‑sarcoma TME heterogeneity, dissect resistance mechanisms and propose integrated, biomarker‑guided therapeutic strategies that can be translated into treatments.

The tumor microenvironment (TME) of epidermal growth factor receptor (EGFR)‑mutant non‑small cell lung cancer (NSCLC) exhibits notable immunosuppressive properties. EGFR tyrosine kinase inhibitors (EGFR‑TKIs) induce dynamic remodeling of the TME. By boosting the infiltration of immune cells such as T cells and dendritic cells and decreasing immunosuppressive elements such as tumor‑associated macrophages and regulatory T cells, short‑term TKI treatment can effectively enhance antitumor immunity. However, the TME changes to an immunosuppressive state marked by PD‑L1 upregulation and immune escape with continued therapy and the emergence of resistance. This creates a transient immunotherapy window period during EGFR‑TKI treatment, when immune checkpoint inhibitors may achieve optimal efficacy. It is essential to identify and take advantage of this window in order to enhance treatment results. The present review highlights the importance of understanding TME dynamics in EGFR‑mutant NSCLC to optimize combination strategies and guide future therapeutic development.

Lung cancer remains a significant global health challenge, with metastatic progression being the leading driver of mortality. Organoid technology provides a tractable, physiologically relevant platform to model key aspects of lung cancer metastasis in vitro. The present review summarized methodologies for constructing and interrogating these models, covering tissue sources, culture modalities, gene editing and in vivo transplantation; applications in studying metastatic mechanisms, drug screening and capturing intra‑ and intertumoral heterogeneity are also highlighted. Persistent challenges include standardizing derivation and culture conditions, improving preservation of tumor‑microenvironmental interactions, expanding immune‑competent and vascularized models, and addressing scalability, cost, and regulatory and ethical considerations for clinical translation. Future directions include integrating multi‑omics approaches and spatial profiling, leveraging artificial intelligence for image and response analytics, advancing immune‑organoid models and establishing shared standards, reference materials and reporting guidelines to enhance reproducibility and clinical impact.

Subsequently to the publication of the above paper, a concerned reader has drawn to the Editor's attention that, for the immunohistochemical data shown in Fig. 2E, the same data panel had apparently been included for the 'ZEB1/Con' and 'SEB2/Min' experiments. In addition, for the Snail2 experiments shown in Fig. 3A, the Snail Con(trol) and Snail Mimi panels looked strikingly similar, even though the intensity of the antibody (red) channel appeared to have been decreased in the Mimi panel. Finally, for the immunohistochemical images shown in Fig. 3C, the E‑cadherin Con(trol) and Scr panels appeared to show a region of overlap, suggesting that these data were derived from the same original source, where the results of differently performed experiments were intended to have been portrayed. Given that it has come to light that this trio of figures had apparently been assembled incorrectly, which might have had an adverse effect on the interpretation of the results and conclusions in the article, 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 29: 1579‑1587, 2013; DOI: 10.3892/or.2013.2267]

The management of nasopharyngeal carcinoma (NPC), a malignancy with pronounced geographic prevalence in Southeast Asia, is undergoing a paradigm shift toward precision medicine driven by innovations in early detection and minimally invasive therapy. Breakthroughs in Epstein‑Barr virus (EBV)‑based screening, such as CRISPR‑associated protein 12a (Cas12a) amplification‑free assays, P85 antibody profiling and T‑cell receptor sequencing, now achieve 97.9% sensitivity and 99.3% specificity, enabling ultra‑early risk prediction 6‑12 months before clinical diagnosis. These advances synergise with multimodal imaging techniques such as narrow‑band imaging and I‑scan virtual chromoendoscopy, which detect sub‑5 mm lesions with 90% sensitivity, revolutionizing screening protocols. Therapeutically, endoscopic nasopharyngectomy (ENPG) exemplifies precision oncology, achieving ≥90% negative resection margins and a 92.1% 5‑year survival rate in early‑stage NPC while preserving key functions (such as swallowing and hearing) and reducing radiotherapy‑related morbidity. Yet, it should be regarded as an indication‑bounded option for carefully selected T1‑T2 disease in experienced centers and does not constitute a universal substitute for radiotherapy. Persistent challenges, including tumor heterogeneity, limited access to advanced technologies in resource‑constrained regions and restrictive ENPG eligibility, underscore the need for artificial intelligence‑driven multi‑omics risk models, portable diagnostic tools and multinational trials to validate long‑term outcomes. By integrating surgical‑immune synergy (such as neoadjuvant programmed cell death protein 1 inhibitors) and equitable implementation strategies, NPC care is transitioning from empirical approaches to a precision framework targeting >80% early diagnosis and >90% functional preservation, offering a roadmap to mitigate the global burden of this regionally concentrated cancer.

Following the publication of the above article, the authors have contacted the Editorial Office to explain that they had noticed that, in Fig. 4 on p. 339, the same western blot data for the ATG5 protein had inadvertently been included for the T24 and the BT5637 cell lines for the 72 h experiments (the lower panels of blots). However, the authors had retained their original data, and were able to identify how this error occurred. The revised version of Fig. 4, now showing the correct data for the ATG5 protein for the 72 h experiment with the BT5637 cell line, is shown on the next page. Note that this error did not affect the overall results and conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the readership of the journal for any inconvenience caused. [Oncology Reports 35: 334‑342, 2016; DOI: 10.3892/or.2015.4335].