Multiple molecular targets involved in inflammation and tumor progression

This term collectively covers a wide array of molecules that mediate the interplay between inflammation and tumor progression. Key components include signaling pathways (NF-κB, JAK-STAT, MAPK), cell surface receptors (cytokine, chemokine, growth factor), transcription factors, and immune cell populations (TAMs, dendritic cells). These components promote tumor cell proliferation, survival, immune evasion, and angiogenesis when dysregulated, while also mediating normal immune defenses. Therapeutic strategies often target these molecules to disrupt pro-tumor inflammation, promote anti-tumor immunity, or address resistance to existing cancer treatments.

Inhibition of signaling pathways (NF-κB, JAK-STAT, MAPK) Antagonism/blockade of receptor interactions (chemokine receptors, cytokine receptors) Immunomodulation (polarizing macrophage phenotype, enhancing antigen presentation)