Inflammation is a physiologic process occurring in response to tissue damage. Already in 1863, Virchow (1, 2), based on the observation that leukocytes infiltrate neoplastic tissues, hypothesized a relationship between inflammation and cancer. The demonstration that inflammation promotes tumor genome instability, cell growth, survival, invasion and angiogenesis has led to the current notion that inflammation is an essential component of malignancies (1) suggesting that it could represent a target for cancer therapy.More recently, the term tumor microenvironment (TME) was used to include both cellular and soluble components which surround and infiltrate the tumor mass (3). The TME is composed of extracellular matrix and stromal cells, including fibroblasts, vessel cells (endothelial cells, pericytes, and smooth muscle cells), and inflammatory leukocytes (lymphocytes, macrophages, dendritic cells, mast cells, and neutrophils), while soluble mediators include a wide spectrum of chemokines, cytokines, and growth factors, which are secreted by both resident tumor and surrounding normal cells as well as by infiltrating immune cells (4-6).It progressively became clear that both the phenotype and the number of infiltrating cells are strongly dependent upon specific chemokines secreted within the TME. Thus, chemokines rapidly became among the most extensively characterized molecules involved in the maintenance and progression of tumor-related inflammation (7).In the five articles included in this Research Topic, different aspects of the most recent lines of research on the field of TME and cancer biology were addressed. The findings are here briefly overviewed with the final aim to provide a stimulating summary of the present knowledge.