Pediatric acute leukemia is one of the most common type of cancer in children. Progress has been made in the past several decades in the treatment success rates of pediatric acute lymphoblastic leukemia (ALL); still 20% of these children are refractory to treatment or relapse following treatment. In AML, the second most common type representing 15-20% of leukemia in children, the prognosis is one of the worst of all childhood cancers and more then 30-40% of children less than 15 years of age will die from the disease. The heterogeneity of leukemia, including the presence of resistant clones, represents a great challenge and currently there are no treatments that address this heterogeneity.
I believe that understanding and monitoring the therapy response at a cellular level in AML patients will provide insights and deeper understanding how to improve treatment of leukemia.
In a recent research project I investigated how conventional chemotherapy affects protein phosphorylation of vital signaling proteins in human leukemic cells. I found that commonly used treatment strategies results in different signaling response on a proteomic level. Now, I want to continue my work to understand how the effect on intracellular cell signaling by chemotherapy agents are involved in the development of therapy resistance.
Additional research projects focus on studying leukemia and hematopoiesis in mouse models developed for both mouse and human cell origin.