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Career Development Program (CDP)

Camille Abboud, MD, and John DiPersio, MD, PhD

The goal is to recruit and support new independent investigators in the field of translational leukemia research. The research initiatives that will be funded by the CDP are expected to have a major translational component, focusing on leukemia etiology, diagnosis, early detection, treatment, or population science.

Eligibility

Junior faculty (Instructor or Assistant Professor) without RO1 or equivalent grant or senior post-doctoral fellows (PhD, MD, or MD-PhD) who have a written commitment from their department chair indicating promotion to Instructor or Assistant Professor by the time of the award also will be eligible.

Awards

One to two awards of $60,000 (direct cost) will be made annually. The second year of funding is contingent upon adequate progress.

Submission Guidelines

The current application cycle is now closed. The next Request for Applications (RFA) will be announced in March 2015 for funding to begin July 1, 2015. For additional information, please contact Amy Abrams at aabrams@dom.wustl.edu

2013 Awardees

 

white.jpg   Brian White, PhD
Project title: Dysregulated splicing in hematological malignancies 

There is emerging data suggesting that mutations of genes involved in RNA splicing are common in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). My research is focused on identifying genes that are differentially spliced by these mutations and determining how altered RNA splicing contributes to MDS or AML pathogenesis.
     
     
j_choi.jpg    Jaebok Choi, PhD
Project title: IFNyR signaling as a therapeutic target to prevent GvHD while preserving GvL

One of the major complications of allogeneic hematopoietic stem cell transplantation is graft-versus-host disease (GvHD). Our recent studies show that the interferon gamma receptor (IFNyR) signaling is required for donor T cells to induce GvHD but not anti-leukemia effect. In this study, we will elucidate the mechanisms by which IFNyR signaling supports GvHD. These data may lead to the ration design of novel therapeutic strategies to mitigate GvHD for patients undergoing allogeneic hematopoietic stem cell transplantation.
 
2014 Awardees

 

 schuettpelz_l   Laura Schuettpelz, PhD
Project title: Elucidating the role of enhanced toll like receptor signaling in myelodysplastic syndrome 

There is increasing evidence that inflammation may contribute to cancer. In this proposal, we focus on toll like receptor signaling. Toll like receptors (TLRs) are genes that recognize pathogens, such as bacteria, and help shape the immune response. Augmented TLR signaling is associated with myelodysplastic syndromes (MDS), a group of blood stem cell disorders that are associated with abnormal blood cell formation and a high risk of progression to acute leukemia. The role of TLRs in the pathogenesis of MDS is not known, however, and in this study we will determine if enhanced TLR expression synergizes with common genetic mutations found in patients with MDS to promote progression of the disease. Ultimately, we hope that drugs targeting TLRs may be useful in the treatment of MDS.
     
     
 spencer.jpg    David Spencer, PhD
Project title: HOX gene regulation in hematopoiesis and AML

The long-term goal of this study is to understand how mutations in acute myeloid leukemia (AML) affect gene regulation and expression to cause cancer. In this project, we focus on HOX genes, which are involved in regulating “self-renewal” in normal stem cells. This capacity is important for normal stem cell function, but abnormal self-renewal contributes to leukemia development and allows cancer cells to continually divide in the bone marrow. Here, we focus on understanding how HOX genes are regulated in normal hematopoietic cells and in leukemia. We will use state-of-the-art genomic approaches to define the regulatory DNA elements that govern HOX gene expression in both normal and leukemic cells, and importantly, whether key differences exist between normal and malignant HOX gene regulation. These studies may lead to strategies for disrupting HOX self-renewal pathways in leukemia cells, which may yield broadly applicable therapeutic approaches for AML.