Acute lymphoblastic leukemia (ALL) is the most common type of childhood cancer, and T-ALL represents 20 % of those, with a peak at 2-5 years of age. Although this neoplastic disorder originates from the thymus, it spreads throughout the whole body and is fatal rapidly without therapy.

Current treatments of T-ALL achieve good survival rates of 90% in children but with severe side effects that alter their quality of life in the long term. Furthermore, about 50% of adolescents and 60% of adults succumb to T-ALL.

We found that abnormal pre-ALL stem cells are 10 to 20 times more resistant to chemotherapy than other leukemic cells, which could explain why the cancer comes back in some children despite treatment.
 
Oncogenic reprogramming and aberrant self-renewal activity are mandatory initiating events in acute leukemias. By uncovering the genetic vulnerabilities of the cells of origin of leukemia and their dependencies on specific niches, we aim to develop novel drug-like compounds, thus translating this mechanistic understanding into novel therapeutic opportunities. 

Early T-cell Precursor Acute lymphoblastic leukemia subtype (ETP-ALL) is associated with resistance to chemotherapy and poor prognosis, especially in adults. Stem cell transplantation is beneficial in a large proportion of patients which suggests high potential for immunotherapy for treatment of ETP-ALL.

Our goal is to uncover tumor specific antigens (TSA), proteins on cancer cells. These proteins are present exclusively on leukemic cells and can be targeted for immunotherapy in ETP-ALL. This will pave the way to developing novel therapeutic vaccines for treatment of ETP-ALLs.