Our research group studies the molecular processes underlying the cross-communication between normal and malignant haematopoiesis and their microenvironment. It has recently been shown that CD34+ CD38- HSPCs can contribute to oncogenic transformation into mature B cell malignancies, such as Chronic Lymphocytic Leukaemia. Similar to normal cells, tumour cells require signals from their surrounding environment to survive and proliferate. Our work has identified vulnerabilities of cancer cells in this cross-talk, which can be exploited therapeutically. We have identified kinases activated in bone marrow stroma cells, which are essential for tumour-associated inflammation and tumour progression. We are now (1) focussed on defining how tumour-host interactions are modulated along tumour-evolution, from the Cell-of-Origin (COO) to lymphoma-stem cells to therapy-refractory disease. These studies are important to (2) fully understand lymphomagenesis and how the tumour microenvironment contributes to drug resistance and minimal-residual disease (MRD) following systemic anti-cancer therapies.