Mind-body therapies (MBTs) are promising forms of treatment for depression and anxiety symptoms in people with cancer, however, their effectiveness has not been compared. The objective of this study is to rank the effectiveness of MBTs for depression and anxiety symptoms in people with cancer. EMBase, PubMed, Cinahl, PsychINFO, IndMED, CSI-NISCAIR, CNKI, Clinicaltrial.gov, ChiCTR, and CTRI were searched until February 2025 for randomised controlled studies in which MBTs were tested in a cancer population. Network meta-analyses were used on the selected studies to rank the reduction in depression and anxiety symptoms compared with usual care. A total of 182 studies which involved 16,835 participants were included. The network meta-analysis showed a statistically significant large effect compared with usual care for biofeedback (standardised mean difference, SMD = -1.18, p = 0.038), spiritual interventions (SMD = -0.98, p = 0.047), and mindfulness-based interventions (MBIs; SMD = -0.87, p < 0.001) for depression symptoms and yoga (SMD = -1.13, p < 0.001), MBIs (SMD = -1.02, p < 0.001), physical relaxation (SMD = -0.93, p < 0.001), qigong/Tai Chi (QTC; SMD = -0.90, p = 0.004) and music therapy (SMD = -0.90, p < 0.001) for anxiety symptoms. The MBTs that should be prioritised are biofeedback, spiritual interventions, and MBIs for depression symptoms and yoga, MBIs, physical relaxation, QTC, and music therapy for anxiety symptoms in people with cancer.

Anticancer drug-induced dermatologic toxicities frequently compromise quality of life and treatment adherence. While diverse strategies have been investigated, evidence patterns across drug classes remain unclear. This scoping review aimed to systematically map clinical studies evaluating preventive and therapeutic interventions for dermatological toxicities-specifically EGFR inhibitor-associated rash, capecitabine-induced hand-foot syndrome (HFS), and multikinase inhibitor-associated hand-foot skin reaction (HFSR)-using a mechanism- and outcome-based framework. Based on the analysis of 51 clinical studies, distinct evidence patterns emerged. For EGFR inhibitor-associated rash, prophylactic strategies using tetracycline- or macrolide-based antibiotics combined with topical corticosteroids consistently reduced grade ≥ 2 events. In capecitabine-induced HFS, both systemic and topical COX-2 inhibition significantly reduced grade ≥ 2 toxicity, while methylcobalamin showed phase III efficacy. For HFSR, barrier reinforcement, COX-2 inhibition, and high-potency corticosteroids were effective. Mechanism-based mapping revealed specific pathophysiological profiles: inflammatory-epithelial for EGFR rash, inflammatory-neuropathic for HFS, and mechanical-vascular-inflammatory for HFSR. Dermatological toxicities associated with anticancer therapies show clear mechanistic divergence and require toxicity-specific preventive strategies. Rather than a one-size-fits-all approach, mechanism-driven and toxicity-specific supportive care represents the most rational and effective strategy for managing these adverse events.

Radiation necrosis (RN) presents a significant challenge in the treatment of pediatric central nervous system tumors. This narrative review synthesizes current evidence on the use of bevacizumab (BEV) for managing pediatric RN, drawing from case reports, retrospective reviews, and prospective clinical trials. While high-quality prospective data remain limited, emerging evidence suggests that BEV may be effective in alleviating both clinical symptoms and radiographic manifestations of RN in pediatric patients. This review explores the pathophysiology of RN, BEV’s mechanism of action, and existing evidence on the use of BEV in pediatric RN. Emerging evidence suggests that bevacizumab may provide symptomatic relief and radiographic improvement in pediatric patients with RN. By addressing current knowledge gaps, the aim is to provide insight into the potential role of BEV in improving outcomes for pediatric patients with RN.

For decades, ovarian cancer (OC) therapy has mainly relied on a regimen of tumor resection followed by treatment with cisplatin and paclitaxel. While this treatment is usually effective initially, resistance to this regimen in OC is widespread and is often the cause of death in OC patients. In the attempt to find new molecular targets for the treatment of chemoresistant OC, understanding the precise mechanisms of chemoresistance remains a paramount task. This review examines the critical roles of the lysosome in the instigation of chemoresistance in OC and explores possible clinical applications for overcoming chemoresistance. Lysosomes contribute to chemoresistance through various mechanisms, including increased lysosomal biogenesis, resulting from the enhanced activity of transcription factor EB, a master regulator of the autophagy-lysosome pathway, which enhances cellular capacity for drug sequestration. Lysosomal exocytosis allows the cell to secrete chemotherapeutic agents from OC cells. Lysosomal autophagy pathways enable OC cells to selectively recycle cell components during chemotherapeutic stress. Finally, lysosomal signaling pathways disrupt various cell death mechanisms such as apoptosis, necroptosis, and ferroptosis, which allow cancer cells to evade death under chemotherapeutic stress. Targeting lysosomal biogenesis, stage-specific autophagy modulation, and lysosome-dependent metabolic vulnerabilities are promising avenues for sensitization of chemoresistant OC cells.