Cancer is fundamentally a highly complex genetic disease characterized by mutations that disrupt the precise regulation of multiple cellular processes, ultimately triggering uncontrolled cell proliferation. These disruptions can affect cellular communication, growth regulation, and response to environmental signals, creating conditions where normal homeostasis is lost and tumor formation occurs. These mutations can specifically affect key regulatory genes involved in apoptosis , DNA repair mechanisms , cell cycle checkpoints , and signaling pathways that maintain tissue homeostasis. The interplay of these genetic alterations not only defines the onset, progression, and heterogeneity of cancer across individuals and tissue types but also influences tumor aggressiveness, response to therapy, and long-term prognosis. While certain genetic predispositions are inherited from parents, the majority of oncogenic mutations arise from external environmental influences. These ...