Authors
Yuxin Wang, Guitong Lv, Xinyue Gao, Zheng Jin, Jiani Huang, Zhongyu Wang
Published in
Frontiers in immunology. Volume 17. Pages 1823423. Epub Jul 10, 2026.
Abstract
Population aging is a major global health challenge and a principal risk factor for cancer. Aging does not simply increase mutational burden; it reshapes tissue homeostasis across genetic, epigenetic, metabolic, immune, and systemic dimensions. Genomic instability, epigenetic drift, mitochondrial dysfunction, and metabolic rewiring collectively establish a tumor-permissive landscape that enhances clonal diversification and lowers the threshold for malignant transformation. Concurrently, accumulation of senescent cells and the senescence-associated secretory phenotype (SASP) remodel the microenvironment, promote immune suppression, and weaken tumor surveillance, further exacerbated by immunosenescence and gut microbiota dysbiosis. Importantly, cancer progression feeds back to accelerate organismal aging. Tumor burden and therapy-induced stress destabilize hematopoietic and non-hematopoietic stem cell niches, disrupt systemic metabolic homeostasis, and induce neuroendocrine reprogramming, thereby amplifying multi-organ functional decline. Aging and cancer therefore constitute a bidirectional and self-reinforcing network rather than a linear cause-effect relationship. In this review, we synthesize mechanistic, clinical, and translational evidence defining the tumor-aging axis and discuss emerging strategies aimed at interrupting this pathogenic cycle.
PMID:
42500653
Bibliographic data and abstract were imported from PubMed on 25 Jul 2026.
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