Onco

Most clinical cancer therapy trials do not specifically consider the effect of patient age on treatment outcomes, and many even exclude older individuals. This is despite the fact that solid cancers are age-associated diseases and that there are many shared hallmarks between biological ageing and cancer. Thus, there is an increasing awareness of the serious gaps remaining in our knowledge of how older adults respond to cancer treatments, particularly immunotherapies. Emerging evidence suggests that it is not only the physiological and immunological changes associated with chronological ageing that impacts cancer treatment, but also those heterogeneous differences that impact treatment outcomes, such as frailty, comorbidities, and more generally, biological ageing. Importantly, it remains unclear which of these factors are negative or positive contributors, as has been illuminated by recent evidence pertaining to the incidence and severity of immune-related adverse events and survival. Much of our information on older patients in this context is essentially anecdotal, mostly deriving from the treatment of older adults in real-world practice or clinical trials that happened to include some older patients. Given the lack of comprehensive articles on the heterogeneity of ageing as a core determinant of cancer treatment outcomes, we briefly consider the state of the art of cancer research and treatment in the older patient, with an emphasis on immunotherapy and geriatric oncology.

In the context of advanced BRAF-mutant melanoma, the treatment landscape has undergone a paradigm shift due to the impact of immune checkpoint inhibitors and BRAF/MEK inhibitors. This article presents three clinically illustrative melanoma cases that served as focal points for in-depth discussions during 12 expert meetings held across Spain. These include a treatment-naïve metastatic melanoma patient, a patient experiencing a recurrence while on anti-PD-1 adjuvant therapy, and a third patient whose melanoma relapsed ≥6 months after the end of adjuvant therapy. The discussions revolved around optimal treatment sequencing, emphasizing the challenges and alternatives discussed in each scenario. The common view aligned towards a nuanced approach that involves navigating the complexities of treatment choices. The conclusions underscore the need for personalized therapeutic strategies and highlight the ongoing challenge of refining real-life evidence-based algorithms for the management of metastatic BRAF-mutant melanoma.

Background: The belief that “sugar feeds cancer” is widespread and has strongly influenced public perceptions, patient behavior, and dietary recommendations, despite uncertainty regarding its scientific validity. This belief largely stems from misinterpretation of the Warburg effect, which describes altered glucose metabolism in cancer cells rather than dietary sugar dependence. The objective of this review was to critically evaluate whether dietary sugar intake directly contributes to cancer development or progression by examining the totality of epidemiological, experimental, and mechanistic evidence. Methods: We conducted a narrative review of human epidemiological studies, experimental animal and cell-based models, and mechanistic investigations published between 1980 and July 2025. Evidence was synthesized across cancer types, sugar sources, and biological pathways, with careful consideration of study design, exposure relevance, and key confounders, including obesity, insulin resistance, and overall dietary patterns. Results: Across cancer types, epidemiological evidence showed predominantly null or inconsistent associations between sugar intake and cancer risk or outcomes, with positive findings largely confined to metabolically susceptible subgroups and often attenuated after adjustment for adiposity and energy intake. Experimental studies suggested potential tumor-promoting effects under non-physiological conditions, while mechanistic data indicated that sugar influences cancer risk indirectly through insulin signaling, inflammation, and metabolic dysfunction rather than direct tumor fueling. Conclusions: Current evidence does not support the hypothesis that dietary sugar directly “feeds” cancer in humans. Overemphasis on sugar avoidance risks nutritional and psychological harm, particularly among cancer patients. Evidence-based guidance should prioritize overall dietary quality, metabolic health, and patient well-being rather than isolated sugar restriction.