Tumor-associated macrophages (TAMs) play a critical role in tumor immune evasion and progression. They are key regulators in the tumor microenvironment (TME), often exhibiting M2-like characteristics. TAMs originate from circulating monocytes and tissue-resident macrophages, and their function is influenced by signals from the tumor and surrounding stromal cells. TAMs contribute to immune evasion by releasing cytokines that suppress effector T cells, attract immunosuppressive cells, and promote tumor growth, angiogenesis, and metastasis. They also influence immune checkpoints, which are crucial for immune evasion. TAMs exhibit functional plasticity, polarizing into M1 or M2 phenotypes based on the TME. M1 macrophages are pro-inflammatory and antitumor, while M2 macrophages are immunosuppressive and pro-tumorigenic. M2-like TAMs are particularly associated with poor prognosis and resistance to immunotherapy. TAMs secrete immunosuppressive factors such as IL-10 and TGF-β, which inhibit T cell and NK cell functions, and promote the development of regulatory T cells (Tregs). They also produce enzymes like Arg-1 and IDO, which further suppress immune responses. TAMs interact with other immunosuppressive cells, such as myeloid-derived suppressor cells (MDSCs) and Tregs, to enhance the immunosuppressive environment in the TME. This interaction is mediated through cytokines, chemokines, and enzymes, which collectively support tumor growth and progression. TAMs also modulate immune checkpoint pathways, such as PD-1/PD-L1, which are critical for immune evasion. Therapeutic strategies targeting TAMs include repolarizing them from M2 to M1, inhibiting their recruitment and activity, and using TAMs as drug delivery vehicles. Epigenetic modifications, metabolic reprogramming, and cellular engineering are promising approaches to modulate TAM function. Despite challenges in clinical application, targeting TAMs offers significant potential for improving cancer treatment outcomes. Understanding the complex interactions between TAMs and the TME is essential for developing effective immunotherapies.Tumor-associated macrophages (TAMs) play a critical role in tumor immune evasion and progression. They are key regulators in the tumor microenvironment (TME), often exhibiting M2-like characteristics. TAMs originate from circulating monocytes and tissue-resident macrophages, and their function is influenced by signals from the tumor and surrounding stromal cells. TAMs contribute to immune evasion by releasing cytokines that suppress effector T cells, attract immunosuppressive cells, and promote tumor growth, angiogenesis, and metastasis. They also influence immune checkpoints, which are crucial for immune evasion. TAMs exhibit functional plasticity, polarizing into M1 or M2 phenotypes based on the TME. M1 macrophages are pro-inflammatory and antitumor, while M2 macrophages are immunosuppressive and pro-tumorigenic. M2-like TAMs are particularly associated with poor prognosis and resistance to immunotherapy. TAMs secrete immunosuppressive factors such as IL-10 and TGF-β, which inhibit T cell and NK cell functions, and promote the development of regulatory T cells (Tregs). They also produce enzymes like Arg-1 and IDO, which further suppress immune responses. TAMs interact with other immunosuppressive cells, such as myeloid-derived suppressor cells (MDSCs) and Tregs, to enhance the immunosuppressive environment in the TME. This interaction is mediated through cytokines, chemokines, and enzymes, which collectively support tumor growth and progression. TAMs also modulate immune checkpoint pathways, such as PD-1/PD-L1, which are critical for immune evasion. Therapeutic strategies targeting TAMs include repolarizing them from M2 to M1, inhibiting their recruitment and activity, and using TAMs as drug delivery vehicles. Epigenetic modifications, metabolic reprogramming, and cellular engineering are promising approaches to modulate TAM function. Despite challenges in clinical application, targeting TAMs offers significant potential for improving cancer treatment outcomes. Understanding the complex interactions between TAMs and the TME is essential for developing effective immunotherapies.