Robert Koch Award 2016, together with Michel C. Nussenzweig
Professor Alberto Mantovani is being recognized for his pioneering work on the link between inflammation and cancer. With his observations that cells of the innate immune system accumulate around certain cancer foci, he opened up an entirely new field of research. Mantovani was able to prove that phagocytes, which are involved in the natural inflammatory response, can be reprogramed in the oxygen-deficient microenvironment of tumors and influence tumor growth. The so-called “tumor-associated macrophages” behave as “corrupted policemen”: they promote cancer cell proliferation, release angiogenic factors that encourage new blood vessels to grow into the tumor and, by releasing enzymes, make the surrounding tissue more permeable to tumor cells, which can promote the formation of metastases. They also contribute to taming effective anti-tumor immunity by triggering molecular breaks called checkpoints in lymphocytes. By characterizing the involved chemokines and their receptors, Mantovani was able to demonstrate how a chronic inflammatory response promotes the development and metastasis of cancer. These studies paved the way to a change in paradigm on the nature of cancer, from a tumor cell-centric view to one that includes corruption and taming of immune cells as an essential component of the “ecological niche” of neoplasia. This shift in vision is now reflected in the development of immunotherapy approaches targeting checkpoints and corrupted policemen.