Inflammatory breast cancer and chest wall disease: The oncologist perspective.

Chest wall inflammatory and lymphangitic breast cancer represents a clinical spectrum and a model disease. Inflammation and the immune response have a role in the natural history of this special clinical presentation. Preclinical models and biomarker studies suggest that inflammatory breast cancer comprises a more important role for the tumour microenvironment, including immune cell infiltration and vasculogenesis, especially lympho-angiogenesis. Across this clinical continuum of the chest wall disease there is an important role of the inflammation cascade. The activation of mature dendritic cells (DCs) through toll like receptors (TLRs) or by inflammatory cytokines converts immature DCs into mature DCs that present specific antigen to T cells, thereby activating them. Maturation of DCs is accompanied by co-stimulatory molecules and secretion of inflammatory cytokines polarizing lymphocytic, macrophages and fibroblast infiltration. It is unknown whether immune cells associated to the IBC microenvironment play a role in this scenario to transiently promote epithelial to mesenchymal transition (EMT) in these cells. Immune and microenvirnment factors can induce phenotypic, morphological, and functional changes in breast cancer cells. We can hypothesize that similar inflammatory conditions in vivo may support both the rapid metastasis and tight tumor emboli that are characteristic of chest wall disease and that targeted anti-inflammatory therapy may play a role in this patient population. The current review will review biological and clinical data of this special condition.