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

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

Promalignant activities	References
TAM-derived factors*
Growth factors	[5–8]
Proteases	[3, 5, 7, 8]
Angiogenic mediators	[3–5, 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	[18–20, 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]

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.

ISSN: 1465-542X