2011 Grant Recipients/Scholars
Attilio Bondanza, MD, PhD
H San Raffaele Scientific Institute
Cell Therapy Of Multiple Myeloma By Genetic Redirection Of T Cells Against Cd44v6
Multiple myeloma, a cancer arising from plasma cells, is the second most common hematologic malignancy, constituting 1 percent of all cancers. Clinical experience with long-term survival after allogeneic HSC transplantation suggests that promising results against multiple myeloma may be achieved through a T cell-mediated immunologic mechanism. Bondanza and colleagues propose to conduct preclinical validation of a novel cell therapy strategy for multiple myeloma treatment based on the genetic redirection of T cells against the tumor antigen CD44v6.
Mettine H.A. Bos, PhD
Leiden University Medical Center, Einthoven Laboratory for Experimental Vascular Medicine
Mechanisms Regulating the Macromolecular Enzyme Complex Assembly in Blood Coagulation
Clotting factors are integral to the blood coagulation process, and disorders in clotting factors can lead to life threatening bleeding disorders. In some cases, clotting factors work together, such as the enzyme factor X and its cofactor, factor V. Bos and coworkers propose to investigate the molecular mechanisms that regulate the assembly of enzyme-cofactor complexes driving blood coagulation.
Swapan Kumar Dasgupta, PhD
Baylor College of Medicine
Signaling Cascade Leading to Phosphatidylserine Exposure in Stored Platelets
Stored platelets undergo changes collectively referred to as the platelet storage lesion. One of the changes is the exposure of the anionic phospholipid phosphatidylserine, or PS, on the cell surface, a hallmark of apoptosis (cell death). Platelets exposing PS are rapidly cleared from circulation, suggesting that this exposure is a signal that prompts macrophages to rid the body of these cells. Dasgupta and colleagues propose that inhibiting PS exposure may help increase the storage time and in vivo recovery of stored platelets.
Eldad A. Hod, MD
Columbia University Medical Center
Effect of Repeat Blood Donation on Atherosclerosis and Cancer Risk in Murine Models
The long-term effects of blood donation on certain disease processes are unknown; however, some researchers have suggested that donation may be cardioprotective and others have proposed that it may reduce the risk of development of certain cancers. Hod will use a mouse model of blood donation that he previously developed to further investigate whether there may be benefits of phlebotomy over time. Hod and colleagues propose to test two hypotheses: that frequent donation is protective, the apoE-knockout mouse model of atherosclerosis and the p53 heterozygous mutant mice that are prone to develop tumors.
Katherine C. MacNamara, PhD
Albany Medical College
IFNγ-Mediated Control of Hematopoietic Stem and Progenitor Cell Differentiation
Interferon-gamma, or IFN-gamma, is a cytokine known for being a suppressor of hematopoiesis. However, recent studies suggest that its roles in the blood system are more complex. Based on her earlier research, MacNamara postulates that IFN-gamma acts differently in less differentiated cells — hematopoietic stem cells and progenitor cells — than in more mature cells, where most previous research on its activity has been conducted. With this NBF grant, MacNamara and colleagues propose to determine the molecular mechanisms that regulate IFN-gamma signaling in distinct populations of HSCs and progenitor cells.
Nilam S. Mangalmurti, MD
University of Pennsylvania
Role of Red Cell Advanced Glycation End products in Endothelial Dysfunction
Observational studies have found that transfusion of stored red blood cells is associated with multiple adverse outcomes, including increased length of hospital stay, prolonged time on ventilator, infections and mortality. Lung injury, independent of transfusion-related acute lung injury, can occur in critically ill patients receiving RBCs. Mangalmurti and colleagues have recently shown that one consequence of RBC storage may be the formation of advanced glycation end-products, or AGEs, on erythrocyte membranes, and that RBCs that have undergone AGE modification can induce oxidative damage in lung cells through a receptor for AGE. With this NBF grant, she proposes to investigate the mechanism of AGE formation on RBCs and look for ways to prevent it.
NBF grants are funded through the generous contributions of NBF Council on Research & Development (CORD) members:
Abbott Laboratories
American Red Cross
Blood Systems/United Blood Services
CaridianBCT (Formerly Gambro BCT)
Fenwal Inc.
Haemonetics Corporation
ITxM
New York Blood Center
Novartis Diagnostics
Ortho-Clinical Diagnostics
Pall Medical
1985 - 2010 Scientific Research Grant Recipients/Scholars