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International Journal of Endocrinology
Volume 2015, Article ID 705169, 8 pages
Review Article

Tumor-Associated Mast Cells in Thyroid Cancer

1Department of Molecular Medicine and Medical Biotechnology (DMMBM), University of Naples Federico II, 80131 Naples, Italy
2Institute of Endocrinology and Experimental Oncology (IEOS), CNR, “G. Salvatore”, 80131 Naples, Italy
3Department of Translational Medical Sciences (DiSMeT), University of Naples Federico II, 80131 Naples, Italy
4Center for Basic and Clinical Immunologic Research (CISI), University of Naples Federico II, 80131 Naples, Italy

Received 24 April 2015; Revised 16 June 2015; Accepted 15 July 2015

Academic Editor: Janete Cerutti

Copyright © 2015 Carla Visciano et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


There is compelling evidence that the tumor microenvironment plays a major role in mediating aggressive features of cancer cells, including invasive capacity and resistance to conventional and novel therapies. Among the different cell populations that infiltrate cancer stroma, mast cells (MCs) can influence several aspects of tumor biology, including tumor development and progression, angiogenesis, lymphangiogenesis, and tissue remodelling. Thyroid cancer (TC), the most frequent neoplasia of the endocrine system, is characterized by a MC infiltrate, whose density correlates with extrathyroidal extension and invasiveness. Recent evidence suggests the occurrence of epithelial-to-mesenchymal transition (EMT) and stemness in human TC. The precise role of immune cells and their mediators responsible for these features in TC remains unknown. Here, we review the relevance of MC-derived mediators (e.g., the chemokines CXCL1/GRO-α, CXCL10/IP-10, and CXCL8/IL-8) in the context of TC. CXCL1/GRO-α and CXCL10/IP-10 appear to be involved in the stimulation of cell proliferation, while CXCL8/IL-8 participates in the acquisition of TC malignant traits through its ability to induce/enhance the EMT and stem-like features of TC cells. The inhibition of chemokine signaling may offer novel therapeutic approaches for the treatment of refractory forms of TC.