Lung cancer (LC) is the leading cause of cancer mortality worldwide. Beyond pharmacological advances, lifestyle interventions such as exercise and nutrition have emerged as valuable adjuvant strategies. Preclinical and translational studies suggest that exercise may modulate molecular and immune pathways relevant to tumor biology, whereas clinical studies support benefits in functional capacity, symptom burden, and quality of life in selected patients with LC. In surgical candidates, prehabilitation focusing on exercise and nutritional optimization improves postoperative outcomes; in unresectable or advanced stages, exercise maintains functionality and mitigates symptoms. Nutritional intervention is critical because malnutrition and sarcopenia are common and negatively affect prognosis. Early screening with tools followed by structured nutritional support, including oral nutritional supplements or, when clinically indicated, enteral nutrition, is recommended. Mediterranean dietary patterns have been associated with a lower risk of cancer, including LC, whereas evidence for improved clinical outcomes after an LC diagnosis remains limited. This narrative review summarizes the physiological rationale, clinical evidence, and practical application of exercise and nutritional interventions across the lung cancer care pathway, while distinguishing direct clinical evidence from preclinical and indirect evidence.

Ferroptosis is a distinct form of regulated cell death that is characterized by iron-dependent oxidative damage and the excessive accumulation of lipid peroxides within cellular membranes. Increasing evidence indicates that ferroptosis is closely associated with tumor initiation, progression, metastasis, and resistance to anticancer therapies. This form of cell death has consequently attracted considerable attention as a potential therapeutic mechanism in a range of malignancies, particularly breast and gynecological cancers. Circular RNAs (circRNAs) are a diverse group of non-coding RNA molecules distinguished by their covalently closed circular structures and remarkable stability. Accumulating evidence has established circRNAs as important regulators of cancer-associated molecular processes at the post-transcriptional level. In the context of ferroptosis, circRNAs may modulate cellular susceptibility to oxidative cell death through several mechanisms, including sequestration of microRNAs, interactions with RNA-binding proteins, and regulation of signaling networks and genes involved in iron metabolism, lipid homeostasis, antioxidant defense, and redox balance. This review provides an overview of the fundamental molecular mechanisms underlying ferroptosis and examines the emerging roles of circRNAs in regulating ferroptotic responses across breast, ovarian, cervical, and endometrial cancers. Particular emphasis is placed on the molecular interactions through which circRNAs influence ferroptosis-associated pathways and on their potential utility as diagnostic, prognostic, and therapeutic biomarkers. The interplay between circRNAs and ferroptosis represents an important area of cancer research, because it may provide new insights into tumor biology and reveal previously unexplored opportunities for precision therapeutic intervention. Nevertheless, further mechanistic investigations, comprehensive in vivo studies, and well-designed clinical investigations are required to establish the translational relevance of these findings and determine whether circRNA-ferroptosis regulatory networks can be effectively exploited in clinical oncology.

Vitiligo-like depigmentation (VLD) arising under immune checkpoint blockade in melanoma is associated with objective tumour response and substantially longer survival. Its prognostic value is not coincidental: depigmentation and tumour regression share a CD8[+] effector programme directed at melanocyte differentiation antigens and recruited through the IFN-γ-CXCL9/CXCL10-CXCR3 axis, an axis independently required for the efficacy of PD-1 blockade. The depigmenting lesion is therefore an accessible compartment in which the antitumour effector response could, in principle, be measured directly. This opportunity is currently unexploited: VLD is graded by inspection, and its molecular correlates are sought almost exclusively in plasma, where a locally generated chemokine signal is diluted into a whole-body average confounded by tumour burden, concurrent immune-related adverse events and corticosteroid exposure. Paired-matrix data from spontaneous vitiligo show that the same chemokines discriminate active from stable depigmentation several-fold in lesional skin interstitial fluid whilst discriminating poorly in serum from the same patients, a finding not yet tested in the ICI setting. Building on this observation as an explicit hypothesis, we reframe the problem as one of matrix selection, pre-analytical control and analytical validation: we compare skin-proximal and systemic matrices against tumour biopsy and circulating tumour DNA, define the pre-analytical variables that are peculiar to oncology, and outline a translational roadmap by which a validated cutaneous assay could convert a visible prognostic sign into a quantitative, early and repeatable readout of antitumour immunity.

Non-small cell lung cancer (NSCLC) remains one of the leading causes of cancer-related mortality worldwide. Although immune checkpoint inhibitors (ICIs) have significantly improved outcomes in patients with unresectable stage III and advanced disease, the lack of robust predictive biomarkers continues to limit patient selection and treatment optimization. Circulating tumor DNA (ctDNA) has emerged as a minimally invasive and dynamic biomarker that enables comprehensive tumor profiling. In this review, we summarize recent advances in ctDNA detection technologies, including quantitative PCR, digital PCR, and next-generation sequencing approaches, and discuss their clinical applications in immunotherapy. We highlight the role of ctDNA in pre-treatment stratification to identify patients most likely to benefit, as well as its utility in real-time monitoring of therapeutic response and disease progression. Furthermore, we discuss emerging high-sensitivity techniques and multi-omics integration strategies that may further enhance the precision of ctDNA-based analysis. Overall, ctDNA holds significant potential to refine clinical decision-making and advance personalized immunotherapy in unresectable and advanced NSCLC.