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Understanding the interplay between tumour microenvironment and cancer cells is an active research area that holds many promises for identifying stroma-derived paracrine drivers of tumour growth or progression that may thus represent possible therapeutic targets.
Pancreatic ductal adenocarcinoma (PDAC), the most common and almost invariably deadly pancreatic tumour, is characterised by a dense tumour stroma that contains a heterogeneous population of cells including stellate cells, fibroblasts, smooth muscle cells, endothelial cells, and a number of inflammatory and immune cells such as dendritic cells and macrophages.1 Indeed, infiltration by immune cells is a hallmark of most forms of malignancy and tumour-associated macrophages (TAMs) represent key regulators of the interplay between immune system and cancer, usually fostering rather than restraining tumour growth.2
TAMs produce a number of potent angiogenic and lymphoangiogenic factors, cytokines, and proteases all of which may potentiate neoplastic progression and tissue invasion, as also indicated by the therapeutic effect of macrophage depletion in specific tumour models.2 Recent evidence suggests that TAM-derived inflammatory components may also act on tissue cells to promote tumourigenesis. For …