Researcher - Michele Redell, MD PhD
Facility - Baylor College of Medicine
Location - Houston, TX
Amount - $50,000.00
Biography: Michele Redell, MD PhD, is an Associate Professor of Pediatric in the Section of Hematology-Oncology at Baylor College of Medicine and Texas Children’s Cancer and Hematology Center. She is a physician-scientist caring for children with leukemia and running a research laboratory focused on acute myeloid leukemia (AML). The goal of her lab’s research is to understand and overcome the processes that allow AML cells to withstand very toxic chemotherapy drugs. Because AML is such a diverse disease that is difficult to replicate with standard research cell lines, her lab studies leukemia samples that are donated by patients and their families for research. Dr. Redell is also involved in clinical research studies through her leadership position in the Children’s Oncology Group Myeloid Diseases Committee. Her ultimate objective is to translate discoveries in the lab to new treatment opportunities for patients.
Lay Description: Children with acute myeloid leukemia (AML) still face a bleak outlook. They endure very intensive and toxic chemotherapy, sometimes with a bone marrow transplant, and still almost half will have the disease come back. Our lab is dedicated to understanding how the AML cells that survive chemotherapy are different from the cells that are eliminated. We recently performed a study of AML samples collected from children at diagnosis and relapse. We identified 32 genes that distinguished cells that survived chemotherapy from cells that did not. One of those genes makes a signaling protein called MIF, and another gene makes the receptor, CD74, that MIF stimulates. We confirmed that some AML cells do indeed make a lot of MIF and CD74. Now we want to know what this pair of proteins does in AML. Our hypothesis is that MIF helps AML cells survive stresses like chemotherapy, and that preventing MIF from stimulating CD74 will make chemotherapy work better. Our first goal is to determine how MIF affects AML cells. Our second goal is to compare the effectiveness of chemotherapy by itself and in combination with an anti-MIF drug. Should this project be successful, we will have compelling evidence to support the clinical development of novel drugs targeting MIF.
Researcher - Margarida Santos, PhD
Facility - The University of Texas MD Anderson Cancer Center
Location - Houston, TX
Amount - $50,000.00
Biography: Dr. Santos received her undergraduate and master’s degrees from the University of Lisbon School of Sciences, in Portugal, and her Ph.D. in Biomedical Sciences from the Medical School at the University of Lisbon. She came to the U.S. as a visiting fellow at the University of Pennsylvania Medical School in 2007 and began her postdoctoral fellowship at the National Cancer Institute of the National Institutes of Health in 2008. In She was recruited to the University of Texas MD Anderson Cancer Center in 2015 to join the Department of Epigenetics and Molecular Carcinogenesis, where she currently is an Associate Professor and leads a Research Lab focused on Leukemia and Lymphoma.
Overview - One of the hallmarks of leukemia is unlimited division of blood progenitor cells that lack the capacity to mature into functional cells. Exploring why these cells fail to mature can help researchers develop new therapies to treat the disease. This what Dr. Santos is hoping that her studies on the role of epigenetics in acute myeloid leukemia can aid in developing new treatments for people diagnosed with this deadly disease. The project funded by WES focuses on a type of acute myeloid leukemia common in children and older adults. In this disease, blood cells called blasts multiply but can’t mature into functional blood cells. Patients feel tired and weak and are susceptible to infections. Although some can be treated with chemotherapy and a stem cell transplant, the treatments are toxic and not all patients are eligible.
Using cultured cancer cells, Dr Santos found a protein called SND1 that in preliminary studies, keeps the leukemic cells from maturing in the Petri Dish; when she genetically deletes this regulator or adds a drug that inhibits its function, the leukemia cells see to differentiate and mature normally. She will now continue to further these studies using human cells and mouse models to understand how this is happening and how this can be applied for therapeutic purposes in patients that have this aggressive type of Leukemia.
Do you like this page?