The interplay between driver mutation and oxidative stress in colorectal cancer: from pathogenesis to therapeutics.

Colorectal cancer (CRC) is a multifaceted disease influenced by genetic mutations and environmental factors, especially oxidative stress. Driver mutations are pivotal in CRC initiation and progression and alter key signaling pathways involved in cell proliferation, apoptosis, and genomic stability. Concurrently, oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, plays a crucial role in CRC development by promoting DNA damage, lipid peroxidation, and redox signaling dysregulation. The molecular mechanisms linking driver mutations and oxidative stress pathways underscore their collective or antagonistic impact on CRC heterogeneity, therapeutic responses, and clinical outcomes. Insights into mutation-specific vulnerabilities and redox modulation offer promising avenues for targeted therapies and personalized medicine approaches in CRC treatment. Here, we discuss the intricate interplay between driver mutations and oxidative stress, highlight emerging trends, and propose future research directions to advance our understanding of CRC pathogenesis and optimize therapeutic interventions.