Tumor-associated macrophages (TAMs) are a key component of the tumor microenvironment and play a critical role in tumor progression. They can be classified into two main subtypes: M1 macrophages, which have anti-tumor functions, and M2 macrophages, which promote tumor growth, invasion, and metastasis. TAMs are highly plastic and can switch between these subtypes based on the tumor microenvironment and therapeutic interventions. Understanding TAMs is crucial for developing new cancer therapies, as they are a promising target for treatment. TAMs originate from bone marrow-derived monocytes and can also come from tissue-specific embryonic-derived macrophages. They are influenced by various factors, including tumor-derived soluble molecules, tumor metabolism, and other immune cells. TAMs can be polarized by signals such as CCL2, CSF-1, and complement components, which regulate their functional state. TAMs interact with the tumor microenvironment in complex ways, influencing tumor growth, angiogenesis, and immune responses. M1 macrophages can directly kill tumor cells through cytotoxic mechanisms, while M2 macrophages promote tumor progression by supporting angiogenesis, tissue repair, and immune suppression. TAMs can also promote tumor metastasis by facilitating the migration of tumor cells and by creating a favorable environment for tumor growth. TAMs regulate immune responses by modulating T cell and NK cell activity, and they can suppress antitumor immunity by promoting the differentiation of regulatory T cells and myeloid-derived suppressor cells. TAMs can also be targeted for cancer therapy through various strategies, including blocking monocyte recruitment, targeting TAM activation, reprogramming TAMs to an anti-tumor phenotype, and targeting specific TAM markers. Current research highlights the importance of TAMs in cancer progression and suggests that targeting TAMs could be a promising approach for cancer treatment. However, many key questions remain, including the mechanisms of TAM development and the factors that drive their phenotypic changes in the tumor microenvironment. Future studies aim to develop more effective therapies targeting TAMs to improve cancer treatment outcomes.Tumor-associated macrophages (TAMs) are a key component of the tumor microenvironment and play a critical role in tumor progression. They can be classified into two main subtypes: M1 macrophages, which have anti-tumor functions, and M2 macrophages, which promote tumor growth, invasion, and metastasis. TAMs are highly plastic and can switch between these subtypes based on the tumor microenvironment and therapeutic interventions. Understanding TAMs is crucial for developing new cancer therapies, as they are a promising target for treatment. TAMs originate from bone marrow-derived monocytes and can also come from tissue-specific embryonic-derived macrophages. They are influenced by various factors, including tumor-derived soluble molecules, tumor metabolism, and other immune cells. TAMs can be polarized by signals such as CCL2, CSF-1, and complement components, which regulate their functional state. TAMs interact with the tumor microenvironment in complex ways, influencing tumor growth, angiogenesis, and immune responses. M1 macrophages can directly kill tumor cells through cytotoxic mechanisms, while M2 macrophages promote tumor progression by supporting angiogenesis, tissue repair, and immune suppression. TAMs can also promote tumor metastasis by facilitating the migration of tumor cells and by creating a favorable environment for tumor growth. TAMs regulate immune responses by modulating T cell and NK cell activity, and they can suppress antitumor immunity by promoting the differentiation of regulatory T cells and myeloid-derived suppressor cells. TAMs can also be targeted for cancer therapy through various strategies, including blocking monocyte recruitment, targeting TAM activation, reprogramming TAMs to an anti-tumor phenotype, and targeting specific TAM markers. Current research highlights the importance of TAMs in cancer progression and suggests that targeting TAMs could be a promising approach for cancer treatment. However, many key questions remain, including the mechanisms of TAM development and the factors that drive their phenotypic changes in the tumor microenvironment. Future studies aim to develop more effective therapies targeting TAMs to improve cancer treatment outcomes.