Tumor-associated inflammation

Tumor-associated inflammation refers to the chronic presence and activity of various immune cells—such as macrophages (TAMs), neutrophils (TANs), fibroblasts (CAFs), lymphocytes—and their secreted factors within the tumor microenvironment. This state is characterized by persistent production of cytokines (e.g., IL‑6, TNF‑α), chemokines, prostaglandins, growth factors like VEGF and TGFβ, matrix metalloproteinases (MMPs), and other molecules that collectively promote cancer initiation and progression through several mechanisms: • Inducing DNA damage via reactive oxygen/nitrogen species. • Supporting angiogenesis for nutrient supply. • Facilitating tissue remodeling for invasion/metastasis. • Suppressing anti-tumoral immunity. • Promoting survival signals that resist apoptosis. Chronic unresolved inflammation creates an environment conducive to malignant transformation ("the perfect storm"), supports cancer cell proliferation/survival/invasion at all stages from initiation through metastasis,[1][4] and is now recognized as a hallmark feature across many cancers.[5] While not itself a druggable molecular entity or receptor/target protein—thus not considered a canonical therapeutic target—the pathways driving this process are under active investigation for intervention strategies using anti-inflammatories or immunomodulators.[3]

Other names

Cancer-associated inflammationTumor-promoting inflammationInflammatory tumor microenvironment

Drugs that affect tumor-associated inflammation generally act by: - Inhibiting pro-inflammatory cytokines and chemokines production/release - Blocking inflammatory signaling pathways such as NF-kB and STAT3 activation - Reducing infiltration or activity of pro-tumoral immune cells in the tumor microenvironment