Funding for 2016

Minson-Katherine.pngResearcher - Kathrine Minson  
Facility - Aflac Cancer and Blood Disorders Center Leukemia and Lymphoma Program at Children’s Healthcare of Atlanta
Location - Atlanta, GA
Amount - $50,000.00
Overview - Dr. Minson is an attending physician in the Aflac Cancer and Blood Disorders Center Leukemia and Lymphoma Program at Children’s Healthcare of Atlanta and an Assistant Professor in the Emory University School of Medicine Department of Pediatrics. She earned her BS in biochemistry and molecular biology from Penn State University in 2005 and her MD from the Medical University of South Carolina in 2009. Dr. Minson went on to complete a residency in Pediatrics at Vanderbilt University and a fellowship in Pediatric Hematology-Oncology at the Children’s Hospital Colorado and University of Colorado where she evaluated a novel small molecule inhibitor aimed at the treatment of AML under the guidance of Dr. Doug Graham. She is currently a recipient of a career development award through the Atlanta Pediatric Scholars K12 Program and is continuing her laboratory research efforts focused on understanding mechanisms of leukemic resistance and development of new treatments for patients with AML.

We have developed a new treatment for acute myeloid leukemia (AML) that targets a protein called MERTK and is very effective with minimal side effects in animal models. This new medicine is moving into the clinic for testing in patients but one problem is that although the treatment increases survival in mouse models, in many cases it does not lead to a long-term cure. We will carry out studies aimed at identifying the proteins that are responsible for resistance to the new medicine in some tumors. These proteins might serve as markers so we can identify patients with tumors that will respond to MERTK therapy and/or could be targeted themselves to promote sensitivity to MERTK therapy. Thus, these studies will help us to understand and develop the most effective ways to use the new MERTK-targeted therapy to treat patients with leukemia, allowing for improved outcomes with less toxicity.


Jane_Liesveld.jpgResearcher - Jane Liesveld, MD
Facility - University of Rochester
Location - Atlanta, GA
Amount - $50,000.00
Overview - Dr. Jane Liesveld received her medical degree from the University of Iowa and subsequently completed an Internal Medicine residency and Hematology-Oncology fellowship at the University of Rochester.  Thereafter, she remained on the faculty at the University of Rochester where she is now Professor of Medicine and the clinical director of the Blood and Marrow Transplant program.  Her clinical work focuses on hematologic malignancy therapeutics with emphasis on acute myelogenous leukemia and myelodysplastic syndromes.  Her laboratory focuses on examination of marrow environment effects on normal and leukemic hematopoiesis as relates to adhesion and cell survival mechanisms as well as preclinical examination of anti-leukemia agents.  

The majority of patients diagnosed with acute myelogenous leukemia (AML) relapse after having achieved a complete remission.  It is thought that the bone marrow environment in which leukemia cells arise and multiply protects some of the leukemia stem cells from the effects of chemotherapy.   Finding ways to inhibit the protective effects of the marrow environment on leukemia cells could therefore have importance in improving disease outcomes.  Cell types in the marrow environment which are known to enhance leukemia growth are endothelial cells, the cells which line vessels, and mesenchymal stem cells (MSCs) which can grow into bone, cartilage, or fat cells.  The work in this proposal  will examine whether disrupting the tethers between leukemia cells and endothelial cells and inhibiting endothelial cell and MSC networks that contribute to AML cell survival will enhance destruction of leukemia cells. This will be tested through laboratory models which mimic AML cell interaction with endothelial cells and MSCs in the marrow.  Understanding how these interactions can be disrupted could have therapeutic implications for AML patients. 

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  • published this page in Research Funded 2016-07-02 10:05:24 -0400