A major focus of cancer research has been on the role of chronic inflammation in tumor development. Chronic inflammation can promote cancer by fostering an environment that supports tumor growth, angiogenesis, and immune evasion. This review discusses the mechanisms by which immune cells contribute to tumor progression and explores therapeutic strategies to neutralize these inflammatory processes. Chronic inflammation is a hallmark of cancer, with immune cells playing both pro- and anti-tumor roles. Certain immune cell subsets, when chronically activated, can promote tumor development. However, these cells can also be reprogrammed to neutralize cancer-promoting inflammation, thereby facilitating cancer rejection. For example, macrophages can be reprogrammed from a pro-tumor state to a tumoricidal state, which can help in tumor regression. Similarly, T helper (Th) cells, particularly Th2 cells, can be reprogrammed from a pro-tumor to an anti-tumor state. Tumor-promoting inflammation is driven by various immune cells, including macrophages, T cells, and B cells. These cells secrete cytokines and chemokines that promote tumor growth, angiogenesis, and immune evasion. For instance, Th2 cells can promote tumor growth by secreting IL-4 and IL-13, which activate macrophages and other immune cells that support tumor progression. In contrast, Th1 cells can promote anti-tumor immunity by secreting IFN-γ, which enhances the activity of cytotoxic T cells. Therapeutic strategies to counteract tumor-promoting inflammation include targeting immune checkpoint pathways, such as PD-1/PD-L1, and reprogramming immune cells to shift from a pro-tumor to an anti-tumor state. Additionally, blocking the recruitment of suppressive myeloid cells and enhancing the activity of cytotoxic T cells can help in tumor rejection. These strategies can be combined with conventional therapies such as chemotherapy, radiation, and targeted therapy to improve clinical outcomes. In conclusion, chronic inflammation plays a critical role in cancer development, and targeting inflammatory processes offers promising therapeutic opportunities. By reprogramming immune cells and modulating inflammatory pathways, it is possible to create an anti-tumor environment that enhances the effectiveness of cancer treatments. This approach, while not a standalone solution, can significantly improve the prognosis for cancer patients.A major focus of cancer research has been on the role of chronic inflammation in tumor development. Chronic inflammation can promote cancer by fostering an environment that supports tumor growth, angiogenesis, and immune evasion. This review discusses the mechanisms by which immune cells contribute to tumor progression and explores therapeutic strategies to neutralize these inflammatory processes. Chronic inflammation is a hallmark of cancer, with immune cells playing both pro- and anti-tumor roles. Certain immune cell subsets, when chronically activated, can promote tumor development. However, these cells can also be reprogrammed to neutralize cancer-promoting inflammation, thereby facilitating cancer rejection. For example, macrophages can be reprogrammed from a pro-tumor state to a tumoricidal state, which can help in tumor regression. Similarly, T helper (Th) cells, particularly Th2 cells, can be reprogrammed from a pro-tumor to an anti-tumor state. Tumor-promoting inflammation is driven by various immune cells, including macrophages, T cells, and B cells. These cells secrete cytokines and chemokines that promote tumor growth, angiogenesis, and immune evasion. For instance, Th2 cells can promote tumor growth by secreting IL-4 and IL-13, which activate macrophages and other immune cells that support tumor progression. In contrast, Th1 cells can promote anti-tumor immunity by secreting IFN-γ, which enhances the activity of cytotoxic T cells. Therapeutic strategies to counteract tumor-promoting inflammation include targeting immune checkpoint pathways, such as PD-1/PD-L1, and reprogramming immune cells to shift from a pro-tumor to an anti-tumor state. Additionally, blocking the recruitment of suppressive myeloid cells and enhancing the activity of cytotoxic T cells can help in tumor rejection. These strategies can be combined with conventional therapies such as chemotherapy, radiation, and targeted therapy to improve clinical outcomes. In conclusion, chronic inflammation plays a critical role in cancer development, and targeting inflammatory processes offers promising therapeutic opportunities. By reprogramming immune cells and modulating inflammatory pathways, it is possible to create an anti-tumor environment that enhances the effectiveness of cancer treatments. This approach, while not a standalone solution, can significantly improve the prognosis for cancer patients.