Biomedical Research Foundation Academy Of AthensAcademy Of Athens
Research Highlights :Autophagy orchestrates the regulatory program of tumor-associated myeloid-derived suppressor cells



Panayotis Verginis and colleagues recently published a study in the Journal of Clinical Investigation



Fundamental discoveries made over the last decade, have unequivocally shown that the immune system plays a vital role in tumor development, shifting the attention of cancer therapy from tumor to immune cells. This knowledge led to the new era of cancer immunotherapy, which however promises durable and sustained responses only in small proportion of cancer patients and is often accompanied by severe adverse events. Delineating the function of tumor infiltrating immune cells is of great need as it will shed light into novel targets for therapies. Myeloid derived Suppressor cells (MDSCs), densely accumulate into tumors and potently suppress anti-tumor immune responses promoting tumor development. Targeting MDSCs in tumor immunotherapy has been hampered by lack of understanding on the molecular pathways that govern MDSC differentiation and function. Recently, Dr. P Verginis group identified autophagy as a crucial pathway for MDSC-mediated suppression of anti-tumor immunity (Alissafi T, Hatzioannou A, Journal of Clinical Investigation 2018).  Specifically, MDSCs in melanoma patients and mouse melanoma exhibited increased levels of functional autophagy. Of note ablation of autophagy in myeloid cells, significantly delayed tumor growth and endowed anti-tumor immune responses. Looking to the future, our group aims to focus on innovative methods to efficiently target autophagy in MDSCs. Such an approach could pave the way for the development of new therapies in the field of cancer.


Alissafi T, Hatzioannou A, Mintzas K, Barouni RM, Banos A, Sormendi S, Polyzos A, Xilouri M, Wielockx B, Gogas H, Verginis P. Autophagy orchestrates the regulatory program of tumor-associated myeloid-derived suppressor cells. J Clin Invest. 2018 Jun 19. pii: 120888. doi: 10.1172/JCI120888.