My main research interest has always been the tumour microenvironment. Malignant cells are able to interact with the surrounding normal cells, altering their behaviour and inducing them to promote the progression of the disease. Thus, a better understanding of what mediate this pathological crosstalk is crucial in order to develop effective anti-tumour therapies.
In 2014 I obtained a PhD in Molecular Medicine from the University of Milan, studying the cellular mechanisms involved in the development of bone disease during the progression of multiple myeloma, a blood cancer arising from plasmacells. Later, I was awarded a fellowship from the Italian Foundation for Cancer Research (FIRC) for a project aimed to study the mechanisms used by myeloma cells to communicate with the neighbouring mesenchymal stem cells and to force them to promote tumour growth and the development of drug resistance.
In 2019 I joined Prof. Adam Mead and Dr Bethan Psaila groups in the MRC Molecular Haematology Unit at the WIMM. Here, we are applying single cell multi-omic approaches to investigate how the bone marrow niche is altered during the development of myelofibrosis. Myelofibrosis is a rare but fatal disease in which the uncontrolled expansion of malignant cells leads to the development of harmful scarring ("fibrosis"), destroying the bone marrow. Survival is typically ~5 years and 1 in 5 patients develop leukaemia. Current treatments help symptoms but do not improve survival or reduce fibrosis.
The main goal of this project is to provide a comprehensive picture of the cellular landscape of the normal and myelofibrotic bone marrow architecture, in order to unravel how the altered stroma sustains disease progression and to identify and validate novel therapeutic targets.