Funding for 2014

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Researcher - Chengcheng Zhang, PhD
Facility - University of Texas Southwestern 
Location - Dallas, TX
Amount - $50,000.00
Overview - Dr. Chengcheng (Alec) Zhang earned his B.S. degree in Molecular Biology from the University of Science and Technology of China in 1992 and his Ph.D. in Biochemistry from the University of Illinois at Urbana-Champaign in 1999. He received his postdoctoral training under the mentorship of Dr. Harvey Lodish at Whitehead Institute/MIT, where he started a project on growing hematopoietic stem cells. Dr. Zhang established his independent lab at UT Southwestern Medical Center in 2007. He is studying the function of immune surface molecules including ITIM-containing receptors on stem cells and leukemia. His research aims to develop novel therapies for regenerative medicine and cancer treatment.

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Researcher - David Frank, MD, Phd.
Facility - Dana-Farber Cancer Institute of the Harvard Medical School 
Location - Boston, MA
Amount - $50,000.00

Overview - Dr. Frank was born and raised in Brooklyn, New York, and graduated from Stuyvesant High School.  He received a B.S. in biology from MIT, and then received an MD and PhD in pharmacology from Yale.  Dr. Frank was an intern, resident, and chief resident in internal medicine at Yale-New Haven Hospital, and was a fellow in medical oncology at the Dana-Farber Cancer Institute.  After postdoctoral laboratory training in intracellular signal transduction at Harvard Medical School, he joined the faculty at Dana-Farber where he cares for patients with hematological malignancies, and conducts laboratory research focused on translating scientific advances into new targeted forms of treatment for patients with cancer.

The goal of this project is to develop a novel targeted approach to the treatment of acute myelogenous leukemia (AML).  AML is the most lethal form of leukemia in adults, and only a small fraction of patients are cured of this disease.  Our current treatments were developed decades ago, and are based on highly toxic drugs that kill normal cells as well as leukemia cells.  Our laboratory is focused on understanding the abnormal patterns of gene expression that drive the malignant behavior of leukemia cells, and developing drugs to target these abnormalities directly.  We have identified two key cellular pathways that control gene expression, which are inappropriately activated in AML cells.  Furthermore, we have identified a drug that can be used in patients, which inhibits both of these pathways. To generate the information we need to initiate a clinical trial, we now plan to elucidate the molecular mechanism by which this drug kills leukemia cells and determine its activity in laboratory models of leukemia.  At the end of the funding period, we plan to pursue a clinical trial of this approach in patients with relapsed or refractory AML, as a step forward in developing targeted molecular therapies for this common form of leukemia.


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Researcher - Edmund K. Waller, MD, PhD, FACP
Facility - Winship Cancer Institute of Emory University School of Medicine 
Location - Atlanta, GA
Amount - $50,000.00
Overview - Recent advances in cancer therapy have high-lighted that the patients' own immune system can effectively eradicate their cancer when the "brakes" on anti-cancer immunity are released. The Emory research team has found that treatment of leukemic mice with daily injections of a small peptide cuts the "brakes" on the immune system, boosts anti-leukemia immunity, and leads to durable eradication of cancer. Research funded by the WES Foundation will accelerate clinical development of this novel approach to leukemia immunotherapy.

 

 


huang.pngResearcher - Gang Huang, PhD
Facility - Cincinnati Children's Hospital Medical Center
Location - Cincinnati, OH
Amount - $50,000.00
Overview - White blood cells cancers, acute leukemias (especially acute lymphoblastic leukemia; ALL), are the most common types childhood cancers. While the overall survival rates for ALL approach 90% since standard chemotherapy was applied 40 year ago. However, in about half of these patients their cancer will come back - relapse. There also remains a group of children whose ALL do not respond well to the standard chemotherapy. Therefore, alternative therapies, such as targeted therapies, need to be developed. Recently, we and others identified novel epigenetic tumor suppressor SETD2 mutations and oncogenic NSD2 (MMSET) mutations in both childhood ALL and acute myeloid leukemia (AML). Both SETD2 and NSD2 control histone-H3 lysine-36 methylation (H3K36me). Therefore, we propose a novel epigenetic tumor suppressor/oncogene circuit that functions through control of the leukemia epigenome. We hypothesize that although acute-leukemia-relevant mutations cause reciprocal biochemical effects in SETD2 versus NSD2, the end product of these changes is the same; a reduction in H3K36me3 mark, an accumulation of H3K36me2 mark, and altered gene expression. The proposed research should define functional relationships between SETD2 and NSD2 in the context of acute leukemia, confirm the novel SETD2-H3K36me3 tumor suppressor pathway and identify novel complimentary opportunities for therapeutic intervention on these epigenetic alterations in acute leukemia.