Labs

My research has centered on understanding the signals that direct early B cell development. Specifically, over the last several years, we have focused on understanding how signals induced by DNA damage impact developmental signals in B cells. B cell development occurs through a carefully regulated process that centers on the generation of a mature, non-autoreactive antigen receptor. To produce a mature antigen receptor, B cells must intentionally generate and repair DNA breaks in the antigen receptor genes. The creation of these DNA breaks is highly regulated by cooperative signaling from two surface proteins, the pre-B cell receptor (pre-BCR) and the interleukin-7 receptor. Together these two signals control cell cycle proliferation and arrest, induction of genes required for antigen receptor gene rearrangement, and cell viability.

The Magee lab is working to answer several important questions that surround the causes of childhood leukemia. How do childhood leukemias arise from normal blood forming stem cells? How do leukemia cells hijack normal stem cell programs? Why do childhood and adult leukemias have different mutations? Can we identify and target programs that maintain leukemia cells that are unique to childhood leukemia?

The Schuettpelz lab studies how inflammation regulates hematopoietic stem cells (HSCs) and contributes to the development of hematopoietic malignancies. Inflammatory signals are important for the normal development of the immune system and the response to acute infection or injury, however sustained inflammatory signaling can impair HSC function. Furthermore, inflammatory signals can promote the clonal expansion of mutant HSCs and the development of hematopoietic malignancies. Understanding how both normal and mutant HSCs respond to inflammation is important for identifying strategies to optimize HSCs function and prevent blood cancers.

My academic focus is on the development of safer less toxic methods of hematopoietic stem cell transplantation in children. Toward this, I am investigating reduced intensity transplantation for children with hemoglobinopathy (sickle cell disease and thalassemia) using the best available related or alternate donors.

The principal objective of my laboratory is to identify and define those molecular features that drive leukemogenesis and then use that information to develop rational therapeutic strategies for improving outcomes in acute leukemia.

The lab is most interested in molecular pathways that: 1) are differentially regulated between malignant cells and their healthy counterparts; 2) promote resistance to conventional chemotherapies; and 3) support leukemia stem cell biology.