Inflammation has long been associated with cancer development, progression, and treatment resistance. This review discusses the complex inflammatory tumor microenvironment (TME), highlighting key inflammatory mediators, including inflammatory cells, cytokines, and their downstream pathways. Inflammation-targeted therapies show potential to suppress cancer and enhance the efficacy of other treatments. The review summarizes preclinical and clinical studies to illustrate the translation potential of inflammation-targeted therapies. Inflammation is a key factor in tumor initiation and progression, with chronic inflammation being a known contributor to cancer. Historical theories, such as those proposed by Rudolf Virchow and Alexander Haddow, suggest a link between inflammation and tumor development. The TME is characterized by immune cell infiltration and elevated inflammatory mediators, which can influence tumor development at various stages. Key inflammatory cells in cancer include tumor-associated macrophages (TAMs), tumor-associated neutrophils (TANs), dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), and T lymphocytes. These cells contribute to tumor growth and immune suppression. TANs can promote tumor angiogenesis and suppress antitumor immunity, while TAMs can switch between M1 and M2 phenotypes, influencing tumor progression. DCs play a critical role in antigen presentation and immune response, but their function is often suppressed in the TME. Inflammatory cytokines such as TNF-α, TGF-β, and IL-6 are involved in tumor progression, immune evasion, and metastasis. TNF-α can have both antitumor and protumorigenic effects, while TGF-β promotes tumor growth and immune suppression. IL-6 supports tumor growth and resistance to therapy. ROS, a byproduct of inflammation, can contribute to cancer development by causing DNA damage and promoting cell proliferation. Inflammatory pathways such as eicosanoid signaling and JAK-STAT signaling are critical in cancer progression. COX-2 and PGE2 signaling are involved in immunosuppression and tumor growth, while LOX pathways contribute to tumor-associated inflammation. JAK-STAT signaling, particularly STAT3, is involved in tumor progression and immune evasion. Inflammation-targeted therapies, including COX-2 inhibitors and JAK-STAT inhibitors, show promise in cancer treatment. These therapies can enhance the efficacy of immunotherapies by modulating the TME. The review highlights the potential of targeting inflammation as a strategy for cancer therapy.Inflammation has long been associated with cancer development, progression, and treatment resistance. This review discusses the complex inflammatory tumor microenvironment (TME), highlighting key inflammatory mediators, including inflammatory cells, cytokines, and their downstream pathways. Inflammation-targeted therapies show potential to suppress cancer and enhance the efficacy of other treatments. The review summarizes preclinical and clinical studies to illustrate the translation potential of inflammation-targeted therapies. Inflammation is a key factor in tumor initiation and progression, with chronic inflammation being a known contributor to cancer. Historical theories, such as those proposed by Rudolf Virchow and Alexander Haddow, suggest a link between inflammation and tumor development. The TME is characterized by immune cell infiltration and elevated inflammatory mediators, which can influence tumor development at various stages. Key inflammatory cells in cancer include tumor-associated macrophages (TAMs), tumor-associated neutrophils (TANs), dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), and T lymphocytes. These cells contribute to tumor growth and immune suppression. TANs can promote tumor angiogenesis and suppress antitumor immunity, while TAMs can switch between M1 and M2 phenotypes, influencing tumor progression. DCs play a critical role in antigen presentation and immune response, but their function is often suppressed in the TME. Inflammatory cytokines such as TNF-α, TGF-β, and IL-6 are involved in tumor progression, immune evasion, and metastasis. TNF-α can have both antitumor and protumorigenic effects, while TGF-β promotes tumor growth and immune suppression. IL-6 supports tumor growth and resistance to therapy. ROS, a byproduct of inflammation, can contribute to cancer development by causing DNA damage and promoting cell proliferation. Inflammatory pathways such as eicosanoid signaling and JAK-STAT signaling are critical in cancer progression. COX-2 and PGE2 signaling are involved in immunosuppression and tumor growth, while LOX pathways contribute to tumor-associated inflammation. JAK-STAT signaling, particularly STAT3, is involved in tumor progression and immune evasion. Inflammation-targeted therapies, including COX-2 inhibitors and JAK-STAT inhibitors, show promise in cancer treatment. These therapies can enhance the efficacy of immunotherapies by modulating the TME. The review highlights the potential of targeting inflammation as a strategy for cancer therapy.