Skip to main content

Table 1 Suggested promalignant activities of inflammatory cells, inflammatory cytokines and inflammatory chemokines in breast carcinoma

From: Host microenvironment in breast cancer development: Inflammatory cells, cytokines and chemokines in breast cancer progression: reciprocal tumor–microenvironment interactions

Promalignant activities References
TAM-derived factors*  
   Growth factors [58]
   Proteases [3, 5, 7, 8]
   Angiogenic mediators [35, 7, 8, 20]
   Promalignant chemokines (CCL2, CXCL8; CCL5 – by unidentified leukocytes) [5, 18, 22]
   Reactive oxygen intermediates [3, 5]
   TNF-α [5, 7, 8, 10, 11]
   Immunosuppressive mediators (PGE2, IL-10, TGF-β) [3, 5, 8]
   Others [5]
TAM-derived TNF-α may promote the expression of:*  
   Promalignant chemokines (e.g. CCL5 by breast tumor cells) [8, 9, 25, 27]
   Matrix metalloproteinases, proteases (e.g. by breast tumor cells) [8, 9, 25]
   Reactive oxygen intermediates [8, 9]
   Angiogenic mediators [1, 8, 9]
   Others [1, 8, 9]
Tumor cell-derived and leukocyte-derived CCL5 and CCL2 may promote:  
   Monocyte migration to breast tumors [1820, 25]
   Matrix metalloproteinase expression by monocytic and breast tumor cells [25, 26]
   Angiogenesis/vascularization (may also be induced by CXCL8) [18, 19, 21, 25, 32, 34]
  1. TAM, tumor-associated macrophages; TNF-α, tumor necrosis factor, transforming alpha; PGE2, prostaglandin E2; IL, interleukin; TGF-β growth factor beta. * In general, some in breast carcinoma.