Malignant tumors remain one of the most significant global health challenges and contribute to high mortality rates across various cancer types. The complex nature of these tumors requires multifaceted diagnostic and therapeutic approaches. This review explores current advancements in diagnostic methods, including molecular imaging, biomarkers, and liquid biopsies. It also delves into the evolution of therapeutic strategies, including surgery, chemotherapy, radiation therapy, and novel targeted therapies such as immunotherapy and gene therapy. Although significant progress has been made in the understanding of cancer biology, the future of oncology lies in the integration of precision medicine, improved diagnostic tools, and personalized therapeutic approaches that address tumor heterogeneity. This review aims to provide a comprehensive overview of the current state of cancer diagnostics and treatments while highlighting emerging trends and challenges that lie ahead.

Context: Chronic kidney disease (CKD) is a significant global health issue, characterized by its progressive nature and the limited effectiveness of conventional treatments. Chinese herbal medicine (CHM) has been used for centuries in East Asia to manage CKD by targeting key pathological processes. This review focuses on synthesizing evidence from various studies to explore the potential role of CHM in managing CKD, particularly through classical formulations, individual herbs, and their bioactive compounds with known nephroprotective effects. Evidence Acquisition: The review synthesizes evidence from preclinical studies, randomized controlled trials (RCTs), and meta-analyses to assess the effectiveness of CHM in CKD management. It highlights the use of classical CHM formulations like Liuwei Dihuang decoction, Zhenwu decoction, Shen-Qi-Wan (SQW), and Yu-Quan Wan (YQW), which are based on CHM theory and syndrome differentiation. Additionally, individual herbs such as Astragalus membranaceus, Salvia miltiorrhiza, Rheum officinale, Tripterygium wilfordii Hook F (TwHF), and Cordyceps sinensis are discussed for their nephroprotective bioactive compounds that provide multi-targeted effects, including anti-inflammatory, anti-fibrotic, antioxidant, and immunomodulatory actions. Results: Integration of CHM with standard therapy has shown promising results in improving renal function and reducing proteinuria, especially in patients with CKD and IgA nephropathy (IgAN). Evidence supports the multi-mechanistic actions of CHM, including the potential for its anti-inflammatory, anti-fibrotic, antioxidant, and immunomodulatory effects to positively impact CKD progression. Conclusions: Despite the growing body of evidence supporting the therapeutic value of CHM in CKD management, challenges still exist, such as the standardization of herbal preparations, ensuring safety, and gaining regulatory approval. For CHM to be more broadly integrated into evidence-based nephrology practice, further high-quality clinical research and harmonization of regulatory frameworks will be crucial. Overall, CHM offers a complementary approach to CKD treatment that aligns with classical principles and multi-targeted actions, contributing to a broader global strategy for CKD management.

Background: Renal cell carcinoma (RCC) is the most common malignant tumor of the kidney, with clear cell renal cell carcinoma (ccRCC) representing its predominant subtype. Despite significant advances in targeted and immune therapies, treatment resistance and recurrence continue to pose major challenges, underscoring the urgent need for novel therapeutic strategies. Jing-Si Herbal Tea (JSHT), a traditional Chinese medicine (TCM) formulation, has demonstrated anti-tumor, anti-inflammatory, and antioxidant properties; however, its mechanisms of action in kidney disease and cancer remain poorly understood. Methods: Human proximal tubule epithelial (HK-2) cells were treated with various concentrations of JSHT (0%, 4%, and 8%) for 24 and 48 hours. Cell viability was assessed using the WST-1 assay. The expression levels of cleaved-caspase 3, glutathione peroxidase 4 (GPX4), and solute carrier family 7 member 11 (SLC7A11) were analyzed by western blotting and quantified relative to β-actin. Results: The JSHT significantly reduced HK-2 cell viability in a time- and concentration-dependent manner. Treatment with JSHT resulted in upregulation of cleaved-caspase 3, indicating activation of apoptosis, while concurrently downregulating GPX4 and SLC7A11, which are key regulators of ferroptosis resistance. These findings demonstrate that JSHT induces two forms of regulated cell death — ferroptosis and apoptosis — in renal epithelial cells. Conclusions: The JSHT exhibits antiproliferative effects in HK-2 cells by promoting apoptosis and sensitizing cells to ferroptosis through suppression of GPX4 and SLC7A11. These results provide preliminary mechanistic insights into the effects of JSHT and indicate its potential relevance for future research in RCC. However, validation in RCC-specific models and in vivo systems is necessary. A notable limitation of this study is the use of a non-cancerous renal cell line; thus, the in vitro findings may not fully recapitulate tumor biology. Future studies employing RCC cell lines, patient-derived tumor models, and in vivo validation are warranted to elucidate the therapeutic potential of JSHT as a complementary approach for RCC management.

Mitochondrial Lon peptidase 1 (LONP1) is an ATP-dependent AAA⁺ (ATPases associated with diverse cellular activities) protease that has emerged as a key regulator of mitochondrial proteostasis, with functions extending beyond protein quality control. In addition to degrading misfolded and oxidized proteins, LONP1 coordinates mitochondrial DNA maintenance, metabolic remodeling, and stress-responsive signaling. Recent structural and functional advances have expanded the biological significance of LONP1 beyond protein quality control, highlighting its roles in mitochondrial metabolism, genome maintenance, and stress responses. LONP1 dysregulation is increasingly implicated in cancer, metabolic disorders, neurodegeneration, and aging, where it exerts context-dependent effects on cell survival and disease progression. In cancer, LONP1 supports metabolic plasticity, redox adaptation, and therapeutic resistance, whereas in degenerative conditions, its decline contributes to mitochondrial dysfunction and tissue damage. Here, we synthesize recent insights into the structure, mechanisms, and biological functions of LONP1 and discuss their implications for human disease. We further discuss emerging therapeutic strategies and key challenges for targeting LONP1 in human disease.