Oxidative stress, characterized by the production of reactive oxygen species (ROS), plays a critical role in cancer development by affecting genomic stability and signaling pathways. ROS disrupt cellular homeostasis, contributing to the loss of normal cellular functions and the initiation and progression of various cancers. This review discusses the downstream signaling pathways influenced by oxidative stress, including p53, Keap1-NRF2, RB1, p21, APC, and tumor suppressor genes. Dysregulation of these pathways leads to uncontrolled cell growth, impaired DNA repair, and evasion of cell death, hallmarks of cancer. Therapeutic strategies targeting oxidative stress aim to modulate redox balance and restore cellular homeostasis, enhancing cancer treatment efficacy. Approaches include antioxidant-based treatments, redox-modulating agents, and interventions restoring normal cellular function. Understanding oxidative stress's role in carcinogenesis and targeting this process through therapeutic interventions is crucial for combating various cancers. Research is needed to unravel the complex mechanisms of oxidative stress-related pathways and develop effective strategies for clinical applications. The review also highlights the interplay between oxidative stress and signaling pathways such as MAPK, PI3K/AKT, and Keap1-NRF2, which are critical in cancer progression. Tumor suppressor genes like BRCA1, BRCA2, and NRF2 regulate oxidative stress and are involved in cancer development. Nanotechnology-based treatment strategies, including ROS-scavenging and ROS-generating nanocarriers, offer promising approaches for targeted cancer therapy. Combination therapies and epigenetic modulators also show potential in enhancing cancer treatment. Future research should focus on understanding the complex interactions between oxidative stress and cellular pathways to develop more effective diagnostic and therapeutic interventions.Oxidative stress, characterized by the production of reactive oxygen species (ROS), plays a critical role in cancer development by affecting genomic stability and signaling pathways. ROS disrupt cellular homeostasis, contributing to the loss of normal cellular functions and the initiation and progression of various cancers. This review discusses the downstream signaling pathways influenced by oxidative stress, including p53, Keap1-NRF2, RB1, p21, APC, and tumor suppressor genes. Dysregulation of these pathways leads to uncontrolled cell growth, impaired DNA repair, and evasion of cell death, hallmarks of cancer. Therapeutic strategies targeting oxidative stress aim to modulate redox balance and restore cellular homeostasis, enhancing cancer treatment efficacy. Approaches include antioxidant-based treatments, redox-modulating agents, and interventions restoring normal cellular function. Understanding oxidative stress's role in carcinogenesis and targeting this process through therapeutic interventions is crucial for combating various cancers. Research is needed to unravel the complex mechanisms of oxidative stress-related pathways and develop effective strategies for clinical applications. The review also highlights the interplay between oxidative stress and signaling pathways such as MAPK, PI3K/AKT, and Keap1-NRF2, which are critical in cancer progression. Tumor suppressor genes like BRCA1, BRCA2, and NRF2 regulate oxidative stress and are involved in cancer development. Nanotechnology-based treatment strategies, including ROS-scavenging and ROS-generating nanocarriers, offer promising approaches for targeted cancer therapy. Combination therapies and epigenetic modulators also show potential in enhancing cancer treatment. Future research should focus on understanding the complex interactions between oxidative stress and cellular pathways to develop more effective diagnostic and therapeutic interventions.