Oxidative Stress and its Role in Carcinogenesis.

Oxidative stress, arising from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, is increasingly recognized as a pivotal driver of cancer initiation and progression. Low ROS levels stimulate signaling pathways and proliferation, whereas excessive ROS induces genetic instability and tissue damage. Cancer cells exploit this paradox by modulating their redox state to support survival, metastasis, and therapeutic resistance. This article explores the multifaceted role of oxidative stress in neoplastic initiation, progression, and metastasis, emphasizing molecular mechanisms such as the DNA damage response, epigenetic remodeling, metabolic reprogramming, and replication stress. Therapeutic strategies, including ROS amplification, inhibition of the antioxidant system, and induction of ferroptosis, are discussed as promising approaches for selectively targeting cancer cells. The complexity of redox signaling in neoplasms underscores its potential as both a pathogenic hallmark and a therapeutic vulnerability.