Early researcher

Giuseppe Di Feo


Since I was a student in high school, I have always been fascinated by studying the molecular and cellular bases of disease and cancer, with the aim of offering patients newly therapeutic perspectives. Therefore, I started studying Biological Sciences (B.Sc.) at the University of Naples, and then Biological Sciences with a molecular diagnostic specialization (M. Sc.) at University of Naples Federico II, Italy, where I graduated cum laude in February 2019.

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During the first year of my master's degree, thanks to my classes in hematology and pathophysiology, I became interested in bone marrow and leukemia biology, in particular in bone marrow biology and tumor microenvironment. During my  master’s degree research in the Department of Women, Children and General and Specialized Surgery of the University of Naples Vanvitelli, I had the possibility to work on two different projects related to hematology and oncology, studying the immunosuppressive effects of mesenchymal stromal cells in childhood immune thrombocytopenia, and the role of the ubiquitin proteasome system in pediatric osteosarcoma. As an intern, this  experience fostered both my interest in cancer-related immunology as well as a curiosity towards the mechanisms involved in cancer development. Thus I decided to move to the United States, to the New York University School of Medicine, in the laboratory of Professor Michele Pagano.

As a research assistant, I focused on elucidating the interplay between the ubiquitin proteasome system and innate  immunity in non-small-cell lung cancer (NSCLC), in particular on how EMSY accumulation suppresses the type I interferon response, impairing innate immune signaling and fostering cancer immune evasion.

Then I moved to France, to Saint Louis Research Institute in August 2021, at the University of Paris, to start my PhD studies at the doctoral school of Hematology-Oncogenesis-Biotherapies, as a part of INTERCEPT-MDS.

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I have always been interested in the biological processes, at cellular and molecular levels, that govern the cross-talk of acute myeloid leukemia cells within the cells present in the tumor bone marrow niche and which clone could drive the disease, in MDS and AML IDH mutated.

My aim is to identify the gene expression signatures associated with primary and adaptive resistance to IDH inhibitors at transcriptomic level in MDS and AML, using different multiomic single cell approaches, in order to conduct a drug screening alleviating the resistance to IDH inhibitors, both in vivo and in vitro.