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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.

Tryptophan metabolism in the immune dysregulation of multiple myeloma
Year Awarded: 2007 Type of Grant: Research Fellow Awards
Location: International Institution: University of Turin
Amount: $75,000 Investigator: Francesca Fiore
The immune system response plays a major role in the new therapeutical approaches against multiple myeloma. Recent data point to the relevance of subsets of dendritic cells and lymphocytes that act as negative regulators of immunity. We will investigate whether the IDO+ cell subsets and regulatory T cells are key players in the immune response also in multiple myeloma, as it has been recently demonstrated for solid tumors and acute leukemia.

Multiple Myeloma and Bone: Understanding the Destruction
Year Awarded: 2007 Type of Grant: Research Fellow Awards
Location: United States Institution: Mayo Clinic Rochester
Amount: $75,000 Investigator: Matthew Drake
More than 80% of patients with myeloma have bone damage, including severe bone pain and fractures. Myeloma cells themselves, however, do not destroy bone. Rather they change the activity of the body��_s own bone forming and bone degrading cells. Several factors produced by myeloma cells which can affect bone cells have been identified. The changes induced within bone forming and bone degrading cells, however, have not been determined. This application seeks to identify these changes. Such findings should identify ways in which these bone cell activities can be altered to reduce the skeletal destruction in patients with myeloma.

The Role of c-FLIP in Multiple Myeloma
Year Awarded: 2007 Type of Grant: Research Fellow Awards
Location: United States Institution: Indiana University (Indianapolis)
Amount: $75,000 Investigator: Attaya Suvannasankha
Multiple myeloma (MM) is an incurable blood cancer. Treatments aiming at key proteins which cause drug resistance may improve treatment outcome. A protein called c-FLIP is expressed at abnormally high levels in MM cells and may make the cancer cells resist chemotherapy. Our data suggest that high levels of c-FLIP are caused by a pathway called NFkB. We will check c-FLIP and NFkB protein levels in bone marrow of MM patients to see whether they are linked. We propose to block the NFkB pathway, thereby lowering the level of c-FLIP and evaluate the effects on the growth of MM cells.

Investigating CDH2 function in myeloma plasma cells and myeloma stem cells
Year Awarded: 2007 Type of Grant: Research Fellow Awards
Location: United States Institution: University of Arkansas
Amount: $75,000 Investigator: James Stewart
Multiple myeloma (MM), a cancer of the plasma cell within the blood, is invariably fatal. MM is dependent on interactions with the bone marrow (BM) microenvironment for enhanced growth and survival. Using a technique called microarray, we measured gene expression profiles of MM cells from our patient cohort and identified the gene, CDH2, which is aberrantly expressed in MM plasma cells when compared to normal controls and is reported to interact with cells in the immediate microenvironment. Investigation of CDH2 function will provide insights into the mechanisms by which malignant plasma cells are supported by the BM.

Forward Chemical Genetic Approach to Protein Catabolism in Multiple Myeloma
Year Awarded: 2007 Type of Grant: Research Fellow Awards
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $75,000 Investigator: Sridevi Ponduru
Multiple myeloma cells are uniquely sensitive to drugs which block the elimination of proteins. Unfortunately, only one such drug is currently FDA approved. Our research lab studies multiple myeloma and cellular pathways of protein elimination. Using high-throughput methods and a chemical library of 14,000 molecules, we have identified more than eighty new drugs capable of blocking protein elimination. Importantly, these drugs are toxic to multiple myeloma cells. We seek funding to develop these drugs as new therapeutic agents in multiple myeloma. We will accomplish this goal immediately and collaboratively with both academic chemists and the pharmaceutical industry.

Novel Polymeric Targeting Nanocarrier for the Treatment of Multiple Myeloma
Year Awarded: 2007 Type of Grant: Research Fellow Awards
Location: United States Institution: The Regents of the University of California
Amount: $75,000 Investigator: Juntao Luo
We plan to apply nanotechnology to the treatment of multiple myeloma. The novel nanomedicine consists of an anti-cancer carrying ��_stealth��_ nanoparticle linked to a molecule that bind to an unique receptor on the myeloma cell surface. When injected into the animal or myeloma patient, the nanomedicine will home to and therefore preferentially kill the myeloma cells and spare the normal cells. In this proposal, we plan to construct this novel nanoparticle drug and then test it against myeloma cell lines in cell culture. If successful, we��_ll test it in mice with myeloma.

Identification of Therapeutic Targets in the Non-Canonical NF-kB Pathway
Year Awarded: 2007 Type of Grant: Research Fellow Awards
Location: United States Institution: Mayo Clinic Arizona
Amount: $75,000 Investigator: Jonathan Keats
Multiple myeloma is characterized by the accumulation of plasma cells, which normally help to fight infections, in the bone marrow. We recently identified a genetic pathway called the non-canonical NF-kB pathway that is defective in at least 20% of myeloma patients. Acquired defects in a number of genes within this pathway promote the growth and survival of the cancer cells. The goals of this study are to determine how defects in this pathway contribute the growth and survival of the cancer cells, if additional genes in the pathway are defective, and to identify the ��_Achilles heal��_ of the pathway.

Characterizing lethal and drug-sensitizing Kinome targets in Myeloma
Year Awarded: 2007 Type of Grant: Research Fellow Awards
Location: United States Institution: Mayo Clinic Arizona
Amount: $75,000 Investigator: Rodger Tiedemann
��_Kinase inhibitors��_ are a growing family of successful new anti-cancer drugs. Each drug blocks one or more enzymes in cancer cells. We propose identifying the best target for this family of drugs in Multiple Myeloma, by examining the effects of inhibiting individually every known kinase enzyme (>600) in Myeloma cells. Moreover, we propose to determine which kinase targets best enhance the effectiveness of bortezomib (Velcade) or lenalidomide (Revlimid), two of the most active drugs in Myeloma, in order to develop highly effective synergistic drug combinations. We will investigate drugs that block these targets for potential treatment of Myeloma.

Mechanism of anti-tumor effects induced by allogeneic donor-cell rejection
Year Awarded: 2007 Type of Grant: Research Fellow Awards
Location: United States Institution: Massachusetts General Hospital (The General Hospital Corp.)
Amount: $75,000 Investigator: Toshiki Saito
Bone marrow transplantation (BMT) can cure myeloma. The current theory on the way BMT works is that the donor bone marrow-derived cells recognize myeloma cells as foreign and kill them. However, this effect is linked to a life-threatening complication, where donor bone marrow-derived cells recognize the recipient as foreign and attack. Recently, we observed that BMT patients who rejected their donor cells and therefore did not get the above complication could surprisingly be cured of very advanced myeloma. We created a model using mice to analyze this phenomenon. In this project, I will dissect the mechanisms of this anti-tumor effect.

Osteoblast and their mesenchymal progenitors in myeloma.
Year Awarded: 2007 Type of Grant: Research Fellow Awards
Location: United States Institution: University of Arkansas
Amount: $75,000 Investigator: Igor Entin
Monoclonal gammopathy of undetermined significance (MGUS) is a pre-cancerous state of multiple myeloma, an incurable tumor accompanied with severe bone destruction. Progression of MGUS and low stage myeloma to overt osteolytic disease is accompanied with disappearing of bone building cells ��_ osteoblasts, whereas osteoclasts, the cells, which destroy bone, increase their activity. Recent findings show that osteoblasts from the late stage of myeloma can inhibit myeloma cell growth. Using our human myeloma in mouse model this proposal addresses the hypothesis that interventions, which restore presence of inhibiting osteoblasts in bone, will prevent progression of myeloma and bone damage.

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