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P53 is a protein encoded by the TP53 gene and functions as a tumor suppressor controlling cell cycle regulation, genomic stability and the induction of apoptosis and. Of all children with relapsed Acute Lymphoblastic Leukemia (ALL), about 12% carry alterations affecting TP53 and this represents a strong and independent predictor of treatment failure. To date, little is known about what makes TP53-aberrant leukemias difficult to treat. The aim of this project is to obtain insights in the biology of TP53 deleted or mutated ALL and to identify specific vulnerabilities that can be targeted to provide new therapy options for this ‘very high-risk’ patient group.