Theano Makridou¹, Elena Vlastou², Vasilios Kouloulias³, Efstathios P. Efstathopoulos⁴, Kalliopi Platoni^4,*

Oncology Research, Vol.33, No.12, pp. 3611-3632, 2025, DOI:10.32604/or.2025.069101 - 27 November 2025

Abstract Nanomedicine has evolved significantly over the last decades and expanded its applications in pediatric oncology, which represents a special domain with unique patients and distinct requirements. Τhe need for early cancer diagnosis and more effective and targeted therapies aiming to increase the pediatric patients’ survival rates and minimize the treatment-related side effects to survivors is profound. Nanoparticles (NPs) come as a beacon of hope to provide sensitive cancer diagnostic tools and assist contrast agents’ transport to the malignant tumors. Besides, NPs could be designed to deliver targeted drugs and genes to tumors, minimizing the medicine-related… More >

Yuri A. Piven¹, Danila V. Sorokin², Nastassia A. Varabyeva¹, Alexandra L. Mikhaylova², Fedor B. Bogdanov², Elena V. Shafranovskaya¹, Raman M. Puzanau³, Fedor A. Lakhvich¹, Alexander M. Scherbakov^2,4,*

Oncology Research, Vol.33, No.12, pp. 4049-4072, 2025, DOI:10.32604/or.2025.067832 - 27 November 2025

Abstract Background: The most aggressive forms of breast cancer are characterized by independence from steroid hormones but a strong dependence on growth factors. In such cancer cells, oncogenic receptors, including human epidermal growth factor receptor 2 (HER2), are activated, and their targeted inhibition represents an attractive therapeutic strategy. The study aimed to develop small-molecule potential dual heat shock protein 90 (HSP90)-HER2 inhibitors and evaluate them as anticancer agents in HER2-positive cells. Methods: The research project involved obtaining a series of compounds with potential dual inhibitory activity against HSP90 and HER2 by targeted organic synthesis, which was… More > Graphic Abstract

Minseo Hong, Jea-Hyun Baek^*

Oncology Research, Vol.33, No.10, pp. 2699-2724, 2025, DOI:10.32604/or.2025.067487 - 26 September 2025

Abstract AMP-activated protein kinase (AMPK) is a highly conserved serine/threonine kinase that functions as a central regulator of cellular energy status. In cancer, where metabolic reprogramming enables rapid proliferation and survival under stress, AMPK functions as a metabolic checkpoint that restrains tumor growth by inhibiting biosynthetic pathways and promoting catabolic processes, such as autophagy and fatty acid oxidation. Given its role in opposing many hallmarks of cancer metabolism, AMPK has attracted significant interest as a therapeutic target. This review examines the molecular mechanisms by which AMPK influences tumor progression and evaluates the preclinical and clinical evidence… More >

Akari Fukumoto, Satoru Matsuda^*

Oncology Research, Vol.33, No.9, pp. 2205-2219, 2025, DOI:10.32604/or.2025.062810 - 28 August 2025

Abstract The non-coding RNAs (ncRNAs) are a family of single-stranded RNAs that have become recognized as crucial gene expression regulators in normal and cancer cell biology. The gut microbiota, which consists of several different bacteria, can actively contribute to the regulation of host metabolism, immunity, and inflammation. Roles of ncRNAs and gut microbiota could significantly interact with each other to regulate the growth of various types of cancer. In particular, a causal relationship among ncRNAs, gut microbiota, and immune cells has been shown for their potential importance in the development of breast cancer. Alteration of ncRNA More >

JIAJIA LV, XIAOYOU ZHONG, LIN WANG, WEIFEI FAN^*

Oncology Research, Vol.33, No.7, pp. 1581-1592, 2025, DOI:10.32604/or.2025.060063 - 26 June 2025

Abstract The tumor microenvironment (TME) is a complex and dynamic network comprised of tumor cells, surrounding cellular components, various signaling molecules, and the stroma. Myeloid-derived suppressor cells (MDSCs) are pivotal players in the immunosuppressive landscape of the TME, effectively hindering antitumor immune responses and facilitating tumor progression. Originating from pathologically activated myeloid precursors and relatively immature myeloid cells, MDSCs retain plasticity to further differentiate into other myeloid cells, such as macrophages or dendritic cells, which underpins their heterogeneity and adaptability in response to the TME. In this review, we delve into the plasticity of MDSCs in More >

YUZHENG LI^1,2, LILI YU¹, SHIYAO ZHOU¹, HUA ZHOU^2,3,*, QIBIAO WU^1,2,*

Oncology Research, Vol.33, No.6, pp. 1363-1376, 2025, DOI:10.32604/or.2025.059311 - 29 May 2025

Abstract Background: Non-small cell lung cancer (NSCLC) involves complex alterations in the epidermal growth factor receptor (EGFR) signaling pathway. This study aims to integrate multimodal omics analyses to evaluate and enhance EGFR-targeted therapies. Methods: We reviewed and synthesized omics data—including genomics, transcriptomics, proteomics, epigenomics, and metabolomics data—related to the EGFR pathway in NSCLC, examined the clinical outcomes of current therapies and proposed new treatment strategies. Results: Integrated omics analyses revealed the multifaceted role of EGFR in NSCLC. Transcriptomic analysis revealed gene expression alterations due to EGFR mutations, with upregulation of oncogenes and downregulation of tumor suppressors. Proteomics More >

Anton Tkachenko^*

BIOCELL, Vol.49, No.5, pp. 721-741, 2025, DOI:10.32604/biocell.2025.063301 - 27 May 2025

Abstract Ferroptosis is an iron-driven, phospholipid hydroperoxide-mediated cell death, which has recently emerged as an attractive tool in cancer research due to its ability to govern the anti-tumor immune response. A growing research interest in ferroptosis biology has revealed the contribution of this regulated cell death to multiple diseases. In addition to iron, ferroptosis has been reported to be triggered by multiple heavy metals, which sheds light on the novel aspects of heavy metals-induced cytotoxicity. In this review, the ability of zinc, an essential biogenic element with a wide array of biological functions, to modulate ferroptosis… More >

MOEKA NAKASHIMA, NAOKO SUGA, AKARI FUKUMOTO, SAYURI YOSHIKAWA, SATORU MATSUDA^*

Oncology Research, Vol.33, No.5, pp. 1007-1017, 2025, DOI:10.32604/or.2025.059657 - 18 April 2025

Abstract Malignant tumors are heterogeneous diseases characterized by uncontrolled cell proliferation, invasion, metastasis, and/or recurrence of their malignancies. In particular, cancer stem cells (CSCs) within these tumors might be responsible for the property of invasiveness and/or therapies-resistance. CSCs are a self-renewing, awfully tumorigenic subpopulation of cancer cells, which are notorious for strong chemoresistance and are frequently responsible the aggravated invasion, metastasis, and/or recurrence. Developing targeting therapies against CSCs, therefore, may be deliberated a more encouraging mission for the greater cancer therapy. Innovation for a more potent anti-CSC treatment has been required as soon as possible.… More > Graphic Abstract

AMJAD YOUSUF¹, NAJEEB ULLAH KHAN^2,*

Oncology Research, Vol.33, No.4, pp. 851-861, 2025, DOI:10.32604/or.2025.058956 - 19 March 2025

Abstract Breast cancer is a significant global concern, with limited effective treatment options. Therefore, therapies with high efficacy and low complications, unlike the existing chemotherapies, are urgently required. To address this issue, advances have been made in therapies targeting molecular pathways related to the murine double minute 2 proto-oncogene (MDM2)-tumor proteinp53 (TP53) interaction. This review aims to investigate the efficacy of MDM2 inhibition in restoring TP53 activity in breast cancer cells, as evidenced by clinical studies, reviews, and trials. TP53 is a tumor suppressor and MDM2 facilitates proteasomal degradation of TP53. MDM2 and TP53 activity More > Graphic Abstract

SHUANG ZHAO^1,#, HONGYONG WEN^2,#, BAIQI WANG², QINGLIN XIONG¹, LANXIN LI¹, AILAN CHENG^1,*

Oncology Research, Vol.33, No.4, pp. 795-810, 2025, DOI:10.32604/or.2025.057317 - 19 March 2025

Abstract Approximately half of all cancers have p53 inactivating mutations, in addition to which most malignancies inactivate the p53 pathway by increasing p53 inhibitors, decreasing p53 activators, or inactivating p53 downstream targets. A growing number of researches have demonstrated that p53 can influence tumor progression through the tumor microenvironment (TME). TME is involved in the process of tumor development and metastasis and affects the clinical prognosis of patients. p53 participates in host immunity and engages in the immune landscape of the TME, but the specific mechanisms remain to be investigated. This review briefly explores the More >