The M1/M2 paradigm of macrophage polarization plays a crucial role in tumor progression. M1 macrophages are typically anti-tumor, while M2-polarized macrophages, known as tumor-associated macrophages (TAMs), contribute to pro-tumorigenic outcomes through angiogenesis, lymphangiogenesis, immune suppression, hypoxia induction, tumor cell proliferation, and metastasis. The tumor microenvironment (TME) influences macrophage recruitment and polarization, leading to these pro-tumorigenic effects. Investigating TME-induced macrophage polarization is essential for understanding TAM-related pro-tumor outcomes and developing new therapeutic approaches. Macrophages are myeloid cells that play key roles in the innate immune response, phagocytosis, antigen presentation, and cytokine secretion. They exhibit anatomical and functional diversity and are critical in tissue homeostasis and wound healing. Macrophage polarization is influenced by various factors, including cytokines, growth factors, and environmental signals. The M1 and M2 phenotypes are characterized by distinct surface markers and secretory profiles, but many macrophages exhibit mixed characteristics. Extrinsic polarization, mediated by cytokines from other cells, is a primary method of macrophage polarization. T Helper 1 (TH1) cells secrete IFN-γ, driving M1 polarization, while TH2 cells secrete IL-4 and IL-13, driving M2 polarization. Intrinsic polarization is influenced by the origin of the macrophage, with bone marrow-derived and embryonic macrophages showing different polarization states. Hypoxia, a common feature in solid tumors, drives macrophage recruitment and polarization, with HMGB1 playing a significant role in hypoxia-induced M2 polarization. Inflammation is a critical component of both normal and pathological processes, and macrophages play a central role in its initiation, maintenance, and resolution. In the TME, TAMs are predominantly M2-like, contributing to immune suppression, proliferation, and metastasis. M2 macrophages secrete immunosuppressive molecules, recruit regulatory T-cells, and express PD-L1 and CTLA4 ligands, enhancing immune evasion. They also promote cancer cell proliferation and angiogenesis, and contribute to lymphangiogenesis and metastasis through the secretion of pro-lymphangiogenic factors and the induction of the epithelial-mesenchymal transition (EMT). Understanding the mechanisms of TAM polarization and their role in pro-tumorigenic outcomes is crucial for developing targeted therapies. Targeting TAMs and their pro-tumor activities could potentially improve treatment efficacy and reduce resistance to anti-cancer therapies.The M1/M2 paradigm of macrophage polarization plays a crucial role in tumor progression. M1 macrophages are typically anti-tumor, while M2-polarized macrophages, known as tumor-associated macrophages (TAMs), contribute to pro-tumorigenic outcomes through angiogenesis, lymphangiogenesis, immune suppression, hypoxia induction, tumor cell proliferation, and metastasis. The tumor microenvironment (TME) influences macrophage recruitment and polarization, leading to these pro-tumorigenic effects. Investigating TME-induced macrophage polarization is essential for understanding TAM-related pro-tumor outcomes and developing new therapeutic approaches. Macrophages are myeloid cells that play key roles in the innate immune response, phagocytosis, antigen presentation, and cytokine secretion. They exhibit anatomical and functional diversity and are critical in tissue homeostasis and wound healing. Macrophage polarization is influenced by various factors, including cytokines, growth factors, and environmental signals. The M1 and M2 phenotypes are characterized by distinct surface markers and secretory profiles, but many macrophages exhibit mixed characteristics. Extrinsic polarization, mediated by cytokines from other cells, is a primary method of macrophage polarization. T Helper 1 (TH1) cells secrete IFN-γ, driving M1 polarization, while TH2 cells secrete IL-4 and IL-13, driving M2 polarization. Intrinsic polarization is influenced by the origin of the macrophage, with bone marrow-derived and embryonic macrophages showing different polarization states. Hypoxia, a common feature in solid tumors, drives macrophage recruitment and polarization, with HMGB1 playing a significant role in hypoxia-induced M2 polarization. Inflammation is a critical component of both normal and pathological processes, and macrophages play a central role in its initiation, maintenance, and resolution. In the TME, TAMs are predominantly M2-like, contributing to immune suppression, proliferation, and metastasis. M2 macrophages secrete immunosuppressive molecules, recruit regulatory T-cells, and express PD-L1 and CTLA4 ligands, enhancing immune evasion. They also promote cancer cell proliferation and angiogenesis, and contribute to lymphangiogenesis and metastasis through the secretion of pro-lymphangiogenic factors and the induction of the epithelial-mesenchymal transition (EMT). Understanding the mechanisms of TAM polarization and their role in pro-tumorigenic outcomes is crucial for developing targeted therapies. Targeting TAMs and their pro-tumor activities could potentially improve treatment efficacy and reduce resistance to anti-cancer therapies.