This review explores the role of inflammation in cancer development, from tumor initiation to metastasis, and discusses the potential of inflammation-targeted therapies. Inflammation has been linked to tumor progression through various mechanisms, including the recruitment of inflammatory cells, the production of cytokines, and the activation of intracellular pathways. 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 the tumor microenvironment (TME) by promoting angiogenesis, immune suppression, and tumor growth. Inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta (TGF-β), and interferons (IFNs) play crucial roles in tumor progression. The review also highlights the importance of reactive oxygen species (ROS) and eicosanoid signaling pathways in inflammation-related cancers. Finally, the article discusses the clinical evidence and preclinical studies supporting the potential of inflammation-targeted therapies, emphasizing their potential to enhance the efficacy of other therapeutic modalities.This review explores the role of inflammation in cancer development, from tumor initiation to metastasis, and discusses the potential of inflammation-targeted therapies. Inflammation has been linked to tumor progression through various mechanisms, including the recruitment of inflammatory cells, the production of cytokines, and the activation of intracellular pathways. 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 the tumor microenvironment (TME) by promoting angiogenesis, immune suppression, and tumor growth. Inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta (TGF-β), and interferons (IFNs) play crucial roles in tumor progression. The review also highlights the importance of reactive oxygen species (ROS) and eicosanoid signaling pathways in inflammation-related cancers. Finally, the article discusses the clinical evidence and preclinical studies supporting the potential of inflammation-targeted therapies, emphasizing their potential to enhance the efficacy of other therapeutic modalities.