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MMRF Funded Grants

As the leading funder of multiple myeloma research, the MMRF has supported more than 325 research grants at over 125 institutions worldwide. The MMRF supports innovative research efforts in the most promising areas of multiple myeloma research through several grant-making programs. Please use the filtering options on the left side of this page to sort through the past MMRF grants shown below.

Please note that grant information for 1997-2005 has not yet been uploaded; thank you for your patience as we work to include this information.

Novel Treatment Approaches to Target the RARa2 Positive Myeloma Cell
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: United States Institution: University of Utah
Amount: $200,000 Investigator: Fenghuang Zhan
Multiple myeloma remains largely incurable. We recently found that tumor cells from about 30% of patients with myeloma express the RARa2 gene. Such patients had a shorter survival. Interestingly, ATRA, a vitamin A derivative that has been very successful in the treatment of acute promyelocytic leukemia, selectively kills myeloma cells expressing RARa2, but not those without RARa2 expression. Furthermore, ATRA-induced anti-myeloma activities were associated with down-regulation of Wnt/ beta-catenin signaling pathway, which is important for rapid tumor growth. Therefore, we propose preclinical research to exploit new approaches based on the combination of ATRA and Wnt signal targeting drugs to treat RARa2-positive myeloma.

Mechanisms of Lenalidomide Resistance
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: United States Institution: University of Texas M.D. Anderson Cancer Center
Amount: $200,000 Investigator: Robert Orlowski
Lenalidomide (Revlimid�_�) is one of our best anti-myeloma drugs, and is used in the newly diagnosed, maintenance, and relapsed/refractory settings. Unfortunately, myeloma cells eventually develop drug resistance through as yet poorly understood mechanisms. We have developed novel models of lenalidomide resistance to study this phenomenon, and already used them to identify some of the pathways involved. Additional studies are proposed to further validate the role of these pathways, and to test approaches to suppress them. These will be translated to the clinic to both increase the effectiveness of this drug and overcome resistance, thereby improving the outcomes of myeloma patients.

Targeting Autophagy in Multiple Myeloma
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $200,000 Investigator: James Bradner
The remarkable activity of the proteasome inhibitor bortezomib against multiple myeloma identifies a unique sensitivity of MM cells to chemicals that block protein recycling. This observation resonates with our understanding of MM cells, which uniquely manufacture an extraordinary amount of protein. We have been studying a critical new pathway of protein recycling termed ��_autophagy��_. With an interest in drug discovery, we have screened chemical libraries for inhibitors of autophagy. The drugs we have identified are promising therapeutic agents, and we now wish to study them in model systems of MM. These studies will establish a priority list and rationale for clinical trials.

Molecular mechanisms of intrinsic resistance of myeloma cells to bortezomib
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: United States Institution: Dartmouth College
Amount: $200,000 Investigator: Alexei Kisselev
About 40% of patients with multiple myeloma (a cancer of white blood cells) respond to the drug bortezomib. Why 60% do not respond is unknown. We have hypothesized that resistance is determined by some myeloma cells��_ ability to counteract specific effects of bortezomib inside the cell. Our immediate goal is to test this hypothesis and to validate the results in patients��_ myeloma cells grown in the laboratory. Our ultimate goal is to be able to predict a patient��_s response to bortezomib based on the laboratory analysis of their myeloma cells. Bortezomib could then be given only to patients whom it would help.

Erythropoietin as an anti-Multiple Myeloma Immunomodulating Agent
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: International Institution: Tel Aviv University
Amount: $200,000 Investigator: Drorit Neumann
We have previously shown that the hormone that enhances the production of red blood cells, affects the immunity to a type of blood cancer (multiple myeloma, MM). Here we address the question which immune cells are affected by the hormone, focusing on cells that can bind the hormone (dendritic cells and macrophages). We shall use blood samples of MM patients as well as mouse experimental models of this cancer. The experiments are geared to find out the molecular mechanisms by which the hormone acts on these cells. We expect that the study will open new powerful strategies for MM immunotherapy.

Development of allosteric proteasome inhibitors for the treatment of MM
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: United States Institution: Michigan State University
Amount: $200,000 Investigator: Jetze Tepe
This application is focused on the characterization, optimization and preclinical testing of a new targeted myeloma drug, TCH-018. Preliminary studies indicate that TCH-018 is non-toxic, but shows effective killing of myeloma cells, alone and in combination with other agents. Results from the studies outlined in this proposal will provide immediate support for the further development of this new type of myeloma agents. TCH-018 (or one of its close analogs) will thus have a potential direct impact on the care of myeloma patients within a relatively short time frame.

HDAC inhibitors and BH3 mimetics in resistant/refractory multiple myeloma
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: United States Institution: Virginia Commonwealth University
Amount: $200,000 Investigator: Steven Grant
The purpose of this project is to develop a new approach highly effective in killing multiple myeloma cells, particularly myeloma cells resistant to other agents. This strategy involves combining a new agent (ABT-737) that induces cell death in myeloma cells with HDAC inhibitors, agents that alter gene expression. Preliminary evidence indicates that this strategy effectively kills myeloma cells. In this proposal, we will optimize regimens, define mechanisms of cell killing, and extend findings to include primary myeloma cells and animal models. If successful, this work could lead to new clinical trials combining HDACIs with ABT-737 in patients with resistant myeloma.

Induction of myeloma cell susceptibility to NK cells
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $200,000 Investigator: Roberto Bellucci
Natural Killer are cells present in the immune system that are responsible for the primary response against infections pathogens and malignant transformations. RNA interference (RNAi) is a new powerful tool that introduces small duplexes of RNA into cells to silence the expression of selected genes allowing investigators to study their functions. We used this powerful tool in a large scale using an already established shRNA library to discover genes and pathway that enhance MM susceptibility to the immune system. The current study will characterize the identified pathways with the goal to create new immunotherapeutic approaches in the cure of MM.

Exploring the role of UCH-L1 in the pathogenesis of myeloma
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: United States Institution: Mayo Clinic Rochester
Amount: $200,000 Investigator: Paul Galardy
We identified a protein that is over-produced in multiple myeloma. This protein, called UCH-L1, is particularly abundant in patients whose myeloma carries a specific aggressive genetic aberration. To determine whether UCH-L1 is important in the biology of cancer we developed a mouse model in which it is over-produced in all tissues. These mice have a striking predisposition to B-cell cancers including lymphoma and myeloma-like tumors. We hypothesize that UCH-L1 is important in the development of myeloma and may represent a target for the design of new drugs.

The humanized Multiple Myeloma mouse model
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: International Institution: University Medical Center Utrecht, DLA
Amount: $200,000 Investigator: Anton Martens
Multiple Myeloma (MM) is one of the most common hematological malignancies in adults with approximately 35,000 new patients per year in the US. Despite three decades of research myeloma has remained an incurable disease with a life expectancy of 3-5 years. Treatment is mainly given on an empirical basis. With new drugs becoming available, predictive drug testing for individual patients becomes very important. Animal models that can predict which drug will be active in which patient are essential. We have developed a novel mouse model for this purpose. Using bone marrow stem cells seeded on a small porous particle of 4x4 mm, we can produce human bone under the skin of the mouse, thus creating an ideal ��_human environment��_. We showed that myeloma cells from patients can grow on this bone and form tumors. This unique mouse model can be used to study the pathology of myeloma and for drug testing.

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