Key muscle development occurs early in life, a time when childhood cancer patients are exposed to aggressive multimodal treatments, placing them at great risk for early declines in muscle health and adverse outcomes later in life. The purpose of this review is to provide an overview of the available evidence describing associations between childhood cancer, its treatment, and the impact on muscle health, identifying gaps in current knowledge.

Aging is associated with increased cancer incidence and immunological decline. Given the increased use of immunotherapies for treating cancer, this review focuses on summarizing results from studies conducted in aged mouse models and clinical trials reporting data specifically on aged study participants.

Similar to chronological aging, anthracycline chemotherapy induces an aging-like phenotype in the vasculature (endothelial dysfunction and large elastic artery stiffness), which markedly increases the risk of developing cardiovascular diseases, kidney dysfunction, and cognitive impairment. This review will discuss how select “hallmarks” of aging (e.g., mitochondrial dysfunction, cellular senescence, and dysregulated energy sensing) could be targeted to prevent and/or treat vascular dysfunction with anthracycline chemotherapy.

Patients over 55 years old constitute the majority of the cancer patient population and suffer from increased metastatic burden compared to younger patients. However, it is largely unclear what role aging may play in this disparity. The natural aging process imparts detrimental changes in the extracellular matrices of all organs. These changes promote organ dysfunction, age-related pathologies, and cancer progression. We proffer that the aging process both helps form the premetastatic niche at common organ sites and facilitates metastatic outgrowth at these sites.

Metabolism alterations of glucose, lipid, and amino acid provide cancer cells with energy and substances for metastasis. Meanwhile, non-tumor cells in TME also undergo metabolic reprogramming or respond to metabolites to promote migration and invasion of cancer cells. Understanding metabolic reprogramming during cancer metastasis is helpful for developing new anti-tumor strategy.

Dietary interventions such as caloric restriction, time-restricted feeding, and/or intermittent fasting exert their protective effects on the risk of neoplastic disease via modulation of age-associated changes in the tissue landscape. The latter include, but are not limited to, alterations in metabolism, autophagy, proteostasis, circadian rhythms, DNA methylation, inflammatory markers, and microbiota composition, all of which can contribute to the emergence of conditions favoring survival and selection of altered cell clones, including those with neoplastic potential.

Cancer cells can survive DNA-damaging agents via DNA damage response (DDR). Inhibition of DDR sensitizes cancer cells to DNA-damaging agents, thus overcoming chemo- and radio-resistance.

There is a dynamic, bi-directional relationship between aging and cancer.