Inflammation plays a critical role in cancer progression, as it creates a microenvironment that supports tumor growth, survival, and metastasis. Inflammatory cells, such as macrophages, neutrophils, and dendritic cells, contribute to tumor development by promoting angiogenesis, suppressing immune responses, and facilitating the spread of cancer cells. Tumor cells also exploit inflammatory signaling pathways, including chemokines and selectins, to enhance their invasive and metastatic potential. Chronic inflammation, often associated with infections or tissue damage, can lead to persistent DNA damage and genomic instability, increasing the risk of cancer. Inflammatory processes are tightly regulated, with anti-inflammatory responses counteracting pro-inflammatory signals to maintain tissue homeostasis. However, in cancer, this balance is disrupted, allowing inflammation to promote tumor growth. Tumor-associated macrophages (TAMs), for example, can support tumor progression by producing growth factors and angiogenic molecules. Additionally, chemokines and their receptors are involved in recruiting inflammatory cells to the tumor site and in the metastatic spread of cancer cells. Anti-inflammatory therapies, such as non-steroidal anti-inflammatory drugs (NSAIDs), have shown promise in reducing cancer risk by inhibiting cyclooxygenase (COX) enzymes and reducing inflammatory signaling. Targeting inflammatory pathways, including MMPs and chemokine receptors, may offer new therapeutic strategies for cancer treatment. Understanding the complex interplay between inflammation and cancer is essential for developing effective interventions to prevent and treat malignancies.Inflammation plays a critical role in cancer progression, as it creates a microenvironment that supports tumor growth, survival, and metastasis. Inflammatory cells, such as macrophages, neutrophils, and dendritic cells, contribute to tumor development by promoting angiogenesis, suppressing immune responses, and facilitating the spread of cancer cells. Tumor cells also exploit inflammatory signaling pathways, including chemokines and selectins, to enhance their invasive and metastatic potential. Chronic inflammation, often associated with infections or tissue damage, can lead to persistent DNA damage and genomic instability, increasing the risk of cancer. Inflammatory processes are tightly regulated, with anti-inflammatory responses counteracting pro-inflammatory signals to maintain tissue homeostasis. However, in cancer, this balance is disrupted, allowing inflammation to promote tumor growth. Tumor-associated macrophages (TAMs), for example, can support tumor progression by producing growth factors and angiogenic molecules. Additionally, chemokines and their receptors are involved in recruiting inflammatory cells to the tumor site and in the metastatic spread of cancer cells. Anti-inflammatory therapies, such as non-steroidal anti-inflammatory drugs (NSAIDs), have shown promise in reducing cancer risk by inhibiting cyclooxygenase (COX) enzymes and reducing inflammatory signaling. Targeting inflammatory pathways, including MMPs and chemokine receptors, may offer new therapeutic strategies for cancer treatment. Understanding the complex interplay between inflammation and cancer is essential for developing effective interventions to prevent and treat malignancies.