ITGAM and neoplasm: Therapy resistance may be mediated by the recruitment by tumor cells of tumor associated macrophages and mast cells [40], pro-angiogenic bone marrow-derived cells including CD11b+ Gr1+ myeloid cells [41] and Tie2+ monocytes [42], tumor associated fibroblasts (TAFs) [43] and production of alternative pro-angiogenic factors [44], including FGF-2 [45], interleukin-8 (IL-8) [46], IL-17 [47], and ANG-2 [48].