Inflammation is a part of carefully co-ordinated healing immune exercise to eliminate injurious stimuli. However, in substantial number of cancer types, it contributes in shaping up of robust tumor microenvironment (TME). Solid TME promotes infiltration of tumor associated macrophages (TAMs) that contributes to cancer promotion. TAMs are functionally heterogeneous and display an extraordinary degree of plasticity, which allow 'Switching' of macrophages into an 'M2', phenotype, linked with immunosuppression, advancement of tumor angiogenesis with metastatic consequences. In contrary to the classical M1 macrophages, these M2 TAMs are high-IL-10, TGF-β secreting-'anti-inflammatory'. In this review, we will discuss the modes of infiltration and switching of TAMs into M2 anti-inflammatory state in the TME to promote immunosuppression and inflammation-driven cancer.
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