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Life sciences · Journal article
Experimental and Molecular Pathology · November 2, 2026
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Inflammation is a complex response that is triggered by infections, toxins, irritants, and tissue injury. Although acute inflammation plays an essential role in immune defense and tissue repair, chronic inflammation has been implicated in the development of cancer, malignancies such as multiple myeloma, lymphomas, and leukemias. This review focuses on the most prevalent and molecularly well-characterized hematological malignancies including acute myeloid leukemia, acute lymphoblastic leukemia, chronic lymphocytic leukemia, Hodgkin and non-Hodgkin lymphomas, and multiple myeloma where the crosstalk between NF-κB and inflammation has been most extensively investigated. NF-κB (Nuclear Factor-Kappa B), a family of transcription factors, controls the inflammatory processes through secretion of pro-inflammatory mediators, such as ILs, chemokines, and TNF-α, during cancer progression. Therefore, aberrant NF-κB activation creates a dysregulated inflammatory state that drives key cancerous processes, including tumor development, immune evasion, metastasis, and therapy resistance. This article reviews the mechanism of inflammation and its crosstalk with NF-κB in hematological malignancies. It then examines the therapeutic implications of targeting NF-κB by reviewing both currently approved agents and those in development. In conclusion, the NF-κB signaling pathway plays a crucial role in acute and chronic inflammatory responses and disruptions in this pathway have been demonstrated to drive the pathogenesis of hematological malignancies, making this pathway an attractive therapeutic target.