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Other mechanisms of therapy resistance involve the recruitment of pro-growth cells and molecules to the TME by the cancer cells as the result of tumour hypoxia, such as tumour-associated macrophages [89], tumour-associated fibroblasts (TAFs) [90], Tie2 + monocytes [91], myeloid cells [92], pro-angiogenic bone-marrow-derived cells including CD11b + Gr1 + and the overexpression of alternative angiogenic signaling molecules [93], including a fibroblast growth factor-2 [94], interleukin-8 (IL-8) [95], IL-17 [96], and angiopoietin 2 [97]