Macrophage polarization states in the tumor microenvironment (TME) are critical for tumor progression. M1 macrophages are traditionally considered anti-tumor, while M2-polarized macrophages, or tumor-associated macrophages (TAMs), promote pro-tumorigenic outcomes through angiogenesis, immune suppression, hypoxia induction, and metastasis. The TME influences macrophage recruitment and polarization, leading to these outcomes. Understanding TME-induced macrophage polarization is essential for developing new therapeutic strategies. This review explores current knowledge of TME-induced macrophage polarization and the role of M2 macrophages in tumor progression. Macrophages are myeloid cells essential for the innate immune response. They originate from monocyte precursors and differentiate in response to cytokines and growth factors. Macrophages exhibit diverse functions, including phagocytosis, antigen presentation, and immunomodulation. They play key roles in tissue homeostasis, inflammation resolution, and tissue development. Macrophages also regulate angiogenesis and lymphangiogenesis, which are crucial for tumor metastasis. Macrophage polarization is influenced by various factors, including cytokines, growth factors, hypoxia, and inflammation. M1 macrophages are pro-inflammatory and produce cytokines that inhibit tumor cell proliferation. M2 macrophages are anti-inflammatory and promote tumor growth, angiogenesis, and immune suppression. Macrophage polarization is not fixed and can change based on environmental signals. M2 macrophages can switch to an M1 phenotype or vice versa in response to changes in the TME. Extrinsic polarization is mediated by cytokine signaling from other cells, such as T-helper cells. Hypoxia is a key driver of macrophage recruitment and polarization in the TME. Hypoxia-associated macrophages secrete pro-angiogenic factors, contributing to tumor progression. Intrinsic polarization refers to the origin of macrophages, with some being derived from embryonic sources and others from bone marrow. The developmental origin of macrophages can influence their polarization state. Macrophages play a key role in inflammation, contributing to both the initiation and resolution of inflammatory responses. In the TME, inflammation is linked to leukocyte infiltration and the expression of pro-inflammatory cytokines. Chronic inflammation can lead to DNA damage and tumor progression. TAMs can suppress immune responses by secreting immunosuppressive molecules and interacting with myeloid-derived suppressor cells (MDSCs). TAMs contribute to pro-tumorigenic outcomes, including immune suppression, proliferation, lymphangiogenesis, angiogenesis, and metastasis. M2 macrophages promote tumor growth by secreting pro-angiogenic cytokines and growth factors. They also support lymphangiogenesis, allowing cancer cells to spread. TAMs can resist therapy by increasing the population of M2-like macrophages in the TME and by expressing immune checkpoint ligMacrophage polarization states in the tumor microenvironment (TME) are critical for tumor progression. M1 macrophages are traditionally considered anti-tumor, while M2-polarized macrophages, or tumor-associated macrophages (TAMs), promote pro-tumorigenic outcomes through angiogenesis, immune suppression, hypoxia induction, and metastasis. The TME influences macrophage recruitment and polarization, leading to these outcomes. Understanding TME-induced macrophage polarization is essential for developing new therapeutic strategies. This review explores current knowledge of TME-induced macrophage polarization and the role of M2 macrophages in tumor progression. Macrophages are myeloid cells essential for the innate immune response. They originate from monocyte precursors and differentiate in response to cytokines and growth factors. Macrophages exhibit diverse functions, including phagocytosis, antigen presentation, and immunomodulation. They play key roles in tissue homeostasis, inflammation resolution, and tissue development. Macrophages also regulate angiogenesis and lymphangiogenesis, which are crucial for tumor metastasis. Macrophage polarization is influenced by various factors, including cytokines, growth factors, hypoxia, and inflammation. M1 macrophages are pro-inflammatory and produce cytokines that inhibit tumor cell proliferation. M2 macrophages are anti-inflammatory and promote tumor growth, angiogenesis, and immune suppression. Macrophage polarization is not fixed and can change based on environmental signals. M2 macrophages can switch to an M1 phenotype or vice versa in response to changes in the TME. Extrinsic polarization is mediated by cytokine signaling from other cells, such as T-helper cells. Hypoxia is a key driver of macrophage recruitment and polarization in the TME. Hypoxia-associated macrophages secrete pro-angiogenic factors, contributing to tumor progression. Intrinsic polarization refers to the origin of macrophages, with some being derived from embryonic sources and others from bone marrow. The developmental origin of macrophages can influence their polarization state. Macrophages play a key role in inflammation, contributing to both the initiation and resolution of inflammatory responses. In the TME, inflammation is linked to leukocyte infiltration and the expression of pro-inflammatory cytokines. Chronic inflammation can lead to DNA damage and tumor progression. TAMs can suppress immune responses by secreting immunosuppressive molecules and interacting with myeloid-derived suppressor cells (MDSCs). TAMs contribute to pro-tumorigenic outcomes, including immune suppression, proliferation, lymphangiogenesis, angiogenesis, and metastasis. M2 macrophages promote tumor growth by secreting pro-angiogenic cytokines and growth factors. They also support lymphangiogenesis, allowing cancer cells to spread. TAMs can resist therapy by increasing the population of M2-like macrophages in the TME and by expressing immune checkpoint lig