In a recent review published in Cell Metabolism , researchers present the role of cyclic fasting and fasting-mimicking diets (FMD) in cancer therapy. FMDs have anticancer properties that potentiate conventional therapies and protect normal tissues. In phase 1/2 clinical studies, cyclic FMD was safe, practical, and related to beneficial metabolic and immunomodulatory benefits in cancer patients.
Modifying the extracellular concentration of metabolites such as glucose, amino acids, or fatty acids exerts anticancer effects via tumor cell-autonomous and immune system-dependent pathways. About the review In the present review, researchers discuss existing preclinical and clinical research and biological mechanisms underlying the effects of FND in oncological treatment. Mechanisms underlying the anticancer actions of FMD In hormonal-receptor-expressing breast cancers, FMD-induced growth factor (GF) level reductions suppress the phosphoinositide-3 kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTORC1) axis.
Contrastingly, among triple-negative-type breast cancers (TNBC), starvation activates mTORC1 and PI3K-AKT pathways, increasing tumor sensitivity to chemotherapeutic agents by inhibiting deoxyribonucleic acid (DNA) repair. FMD results in longer remissions with mTORC1 and PI3K-AKT inhibitors. The decrease in glucose obtainability caused by fasting/FMD may induce tumor cells to maximize adenosine triphosphate (ATP) generation by oxidative phosphorylation (OXPHOS.