Abstract
Tumor-associated macrophages (TAMs) are key cells in tumor-associated chronic inflammation, and can promote tumor growth, proliferation, angiogenesis, invasion, metastasis and chemotherapy resistance. Under different circumstances, macrophages can be polarized into classically activated macrophages (M1) and alternatively activated macrophages (M2). Cyclooxygenase 2, nuclear factor-κB, Toll like receptor (TLR) signaling pathway, anoxia, the protooncogene MYC, Notch signaling pathway and cytokines are all involved in the transition of TAMs from M1 to M2 phenotype. The phenotype and function of TAMs vary with tumor progression, so antitumor drug therapies targeting macrophages should depend on the stage of tumors. Key words: Macrophages; Neoplasms; Phenotype
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