Inflammation-Driven Tumorigenesis: Mechanisms, Immune Evasion, and Therapeutic Strategies
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Abstract
Cancer is a complicated disease influenced by genetic, environmental, and immunological factors. Among these, chronic inflammation has emerged as a critical factor in tumor initiation, progression, and metastasis. The inflammatory tumor microenvironment, enriched with cytokines, chemokines, and immune cells, fosters immune evasion, angiogenesis, and genomic instability and key signaling pathways, including NF-κB, STAT3, and COX-2/PGE2, bridge inflammation and oncogenesis, making them promising therapeutic targets. Despite the tumor-promoting effects of chronic inflammation, the immune system also plays a crucial role in immunosurveillance, eliminating malignant cells. However, tumors develop escape mechanisms, such as immune checkpoint activation and recruitment of immunosuppressive cells, enabling survival and metastasis. Current therapeutic strategies target inflammation-driven tumorigenesis through nonsteroidal anti-inflammatory drugs (NSAIDs), cytokine inhibitors, immune checkpoint inhibitors, and combination therapies. Understanding the balance between pro- and antitumor immunity is essential for advancing novel therapeutic interventions. This review highlights recent findings on inflammation-driven cancer progression, the molecular mechanisms involved, and emerging strategies to harness inflammatory pathways for cancer treatment.
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