Reacción a "A study in mice shows that periodic fasting may improve treatment for hormone-dependent breast cancer"

This well-designed and comprehensive study provides valuable insights into how metabolic changes during fasting could enhance hormone therapy in estrogen receptor-positive breast cancer. The authors use a powerful combination of genomic and functional approaches, and the consistent activation of glucocorticoid and progesterone receptor pathways in the different models is a particularly interesting mechanistic finding. These data offer a promising direction for future research on fasting-mimicking strategies or glucocorticoid-based therapeutic approaches.  

However, several important limitations need to be considered when interpreting the results. The work is largely preclinical, and although supported by small patient cohorts, the human data are preliminary and lack control groups. The mouse studies were conducted primarily in immunodeficient models, limiting our ability to assess how fasting or glucocorticoid signalling might interact with the immune system in a clinically relevant setting. Furthermore, key endocrine and pharmacokinetic variables, such as oestrogen levels and exposure to the tamoxifen metabolite, were not measured, so it remains unclear how much of the observed effect reflects direct mechanistic action versus broader hormonal changes. 

Overall, this is an intriguing and insightful study that broadens our understanding of metabolic influences on endocrine therapy, opening the door to promising new lines of research, including whether glucocorticoid-based fasting mimetics could be safely and effectively tested in humans. However, it is still too early to know whether these findings will translate into meaningful benefit for patients, and clinical recommendations should not change until robust human trials have been completed.