Serum uric acid and its metabolism-a vital factor in the inflammatory transformation of cancer.

BACKGROUND

Uric acid (UA) is the terminal product of purine metabolism. Elevated serum uric acid (SUA) levels, resulting from excessive synthesis or impaired excretion, are link to chronic inflammatory stress and increased risks of colorectal, breast, and prostate cancers. Hyperuricemia triggers a cascade of proinflammatory and oxidative responses, establishing a microenvironment conducive to tumorigenesis.

AIM OF REVIEW: This review synthesizes evidence on how hyperuricemia drive inflammation and cancer transformation from global foundational research and clinical practice, elucidate UA metabolism as potential therapeutic strategy for inflammation-associated malignancies.

KEY SCIENTIFIC CONCEPTS OF REVIEW: Hyperuricemia-induced oxidative stress, DNA damage and genomic instability, while simultaneously activating proinflammatory signaling pathways. These interconnected pathways establish a persistent, proinflammatory microenvironment that fosters the transition from inflammation to cancer. Therapeutic strategies targeting UA metabolism (including pharmacologic interventions and dietary modifications) may mitigate chronic low-grade inflammation and reduce the cancer risk associated with hyperuricemia. Dysregulated UA metabolism emerges as a critical modulator linking chronic inflammation with oncogenesis.