This chapter outlines how cancer coopts fundamental physiological programs, such as wound healing, immune regulation, angiogenesis, microbiome interactions, and metabolism, to support malignant growth. Tumors mimic nonhealing wounds: they chronically activate hemostasis, inflammation, fibroblast expansion, ECM remodeling, and angiogenesis, driven by factors such as VEGFA, IL6, G-CSF, and GM-CSF. The tumor microenvironment consists of malignant cells embedded within stroma composed of fibroblasts, endothelial cells, immune cells, nerves, and microbiota. These components interact to promote immune evasion through local, regional, and systemic mechanisms affecting antigen presentation, chemokine signaling, and lymphocyte infiltration. Sustained angiogenesis enables tumors to overcome diffusion limits, while hypoxia selects aggressive, genetically unstable clones. Chronic inflammation, which is mediated by TAMs, neutrophils, senescent cells, and obesity-associated metabolic stress, promotes tumor progression, suppresses adaptive immunity, and generates additional mutations. The microbiome influences carcinogenesis through genotoxicity, inflammation, metabolic signaling, and modulation of therapy response. Microbial composition especially shapes checkpoint inhibitor efficacy. Metabolic reprogramming, including the Warburg effect and altered nutrient utilization, supports proliferation while creating an immunosuppressive, acidic microenvironment. Stromal cells and systemic metabolic disorders, such as obesity, further modulate tumor energetics and immune cell trafficking. Altogether, cancer emerges as a systems-level disease driven by dysregulated regenerative, immune, microbial, and metabolic networks.