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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.

Synergistic Effects of PS-341 (Velcade) and BX471 on Multiple Myeloma
Year Awarded: 2006 Type of Grant: Validation of Novel Compounds
Location: United States Institution: University of Pittsburgh
Amount: Not Available Investigator: Suzanne Lentzsch
Macrophage inflammatory protein-1alpha (MIP-1alpha) is a protein produced by multiple myeloma (MM) cells, which induces proliferation of MM cells, formation of cells that resorb bone tissue, and is partly responsible for bone destruction. BX471 prevents binding of MIP-1alpha to receptors and inhibits the formation of these cells. PS-341 is effective at inhibiting replication of MM cells. We hypothesize that combining both drugs will exert profound anti-myeloma effects and result in inhibition of bone disease, and that targeting two regulators of cell growth will result in an anti-MM effect greater than the sum effect of both drugs, but less toxicity.

Combining Tumor Vaccines with Adoptive Immunotherapy in Myeloma
Year Awarded: 2006 Type of Grant: Validation of Novel Compounds
Location: United States Institution: Johns Hopkins University
Amount: $100,000 Investigator: Ivan Borrello
In multiple myeloma, autologous stem cell transplants are seldom curative. Novel strategies are thus needed. Recently clinical studies using myeloma vaccines and activated immune cells provided significant insight into their efficacy when given alone and suggests that combining therapies could significantly augment anti-tumor immunity. A recent study combining the activated T cells with a pneumonia vaccine significantly augmented vaccine responses. With experience from these prior studies, we thus propose to combine the use of myeloma vaccines with activated T cells in autologous transplants as a strategy to improve myeloma-specific immune responses.

Synergistic Combinations of Targeted Agents for Myeloma
Year Awarded: 2006 Type of Grant: Validation of Novel Compounds
Location: United States Institution: Emory University
Amount: Not Available Investigator: Sagar Lonial
The use of targeted agents such as velcade represents a major advance over the use of standard chemotherapy, but are not universally effective. Combinations of targeted agents have the potential to attack different pathways responsible for cancer cell survival, and represent a new approach as most cancers are dependent upon several pathways. Our lab has generated data indicating that the combination of farnesyl transferase inhibitors with velcade results in more myeloma cell death than when either agent is used alone. We propose to test why this occurs, and to initiate a phase I trial combining these agents.

Effects of JS-K, a GST based NO generator, on MM: therapeutic implications
Year Awarded: 2006 Type of Grant: Research Fellow Awards
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $75,000 Investigator: Tanyel Kiziltepe Bilgicer
Multiple Myeloma (MM) still remains an incurable disease. This is predominantly due to development of drug resistance in tumor cells which eventually leads to relapse of the disease. JS-K is a novel agent that is designed to turn one of the major resistance mechanisms developed by tumor cells to their disadvantage to kill them. The preliminary results presented in this proposal show that JS-K selectively induces death even in MM cells resistant to standard treatments. Here I propose to evaluate the efficacy of JS-K in animal models and take it forward clinically alone and in combination with other conventional and/or novel drugs, to improve treatment of MM.

Therapeutic Targeting of Ire1/XBP-1 in Malignant B Cells
Year Awarded: 2006 Type of Grant: Research Fellow Awards
Location: United States Institution: Stanford University
Amount: $75,600 Investigator: Douglas Feldman
Multiple myeloma arises through the uncontrolled division of B cells, immune cells that specialize in antibody production. The secretory capacity of B cells is sustained by expansion of the endoplasmic reticulum (ER), a cellular compartment where secreted proteins are made. Secretory cells depend for their survival on a signaling pathway called the ER stress response, which expands the ER in response to increased demand. We have identified chemical inhibitors of Ire1, a core component of the ER stress response. We hypothesize that treatment of multiple myeloma cells with these inhibitors will block antibody secretion and cause the selective killing of malignant B cells.

Genomic and Functional characterization of p53 pathway in MM
Year Awarded: 2006 Type of Grant: Research Fellow Awards
Location: United States Institution: Mayo Clinic Arizona
Amount: $75,000 Investigator: Wee Chng
The p53 protein is an important tumor suppressor that coordinates protective responses of the cell against environmental stresses that promote cancer formation. The status of p53 function has not been systematically studied in myeloma. Recently, a novel form of cancer treatment based on stimulating the p53 response has been developed. The effectiveness of this treatment depends on the ability of p53 to exert its function. As this may represent a useful treatment in MM, we aim to characterize p53 function in myeloma and correlating the various functional states with response to this new treatment.

Identification of Novel Targets for T-Cell Immunotherapy of Myeloma
Year Awarded: 2006 Type of Grant: Research Fellow Awards
Location: United States Institution: Fred Hutchinson Cancer Research Center
Amount: $75,000 Investigator: Larry Anderson
T-cells recognizing myeloma can be detected in myeloma patients and can mediate a graft versus myeloma response following allogeneic transplantation, but the lack of defined target antigens other than idiotype has hindered the development of myeloma-specific T-cell immunotherapy. We will identify myeloma antigens recognized by CD8+ T-cells starting with two candidate myeloma antigens: MAGE-C1 (CT-7), a cancer/testis antigen, and B-Cell Maturation Antigen (BCMA), a plasma cell differentiation antigen, both commonly over-expressed in myeloma. We will also identify antigens recognized by myeloma-reactive T-cells from myeloma patients. This work will enable the development of vaccines and adoptive T-cell therapies for myeloma.

Transgenic mouse model of drug development for multiple myeloma
Year Awarded: 2006 Type of Grant: Research Fellow Awards
Location: United States Institution: Mayo Clinic Arizona
Amount: $75,000 Investigator: Michael Sebag
In order to rationally and effectively develop treatments for multiple myeloma, improved pre-clinicla models are needed. Existing mouse models of myelom are woefully inadequate as they do not acurately simulate the clinical picture in humans. We have developed novel transgenic mice that uses somatic hypermutation to activate an oncogene (myc) and reproducibly develop smouldering myeloma. In addition we have crossed these with mice that are engineered to express acivated FGFR3. In contrast to other models, disease is limitted to the bone marrow. We wish to test this model as a as a pre-clinical screening tool for drugs with efficacy against multiple myeloma. We hypothesize that this model will be a more predictive tool in determining active or inactive drugs in the clinical setting.

Novel Natural Products with Potential Therapeutic Uses in Multiple Myeloma
Year Awarded: 2006 Type of Grant: Research Fellow Awards
Location: United States Institution: Mayo Clinic Rochester
Amount: $75,000 Investigator: Jennifer Tibodeau
Multiple myeloma is a uniformly fatal cancer killing about 12,000 individuals annually in the U.S. alone. We have recently discovered that two agents isolated from natural sources, chaetocin and cis-bixin, have impressive and selective anti-myeloma activity in freshly collected patient bone marrow cells, making them attractive agents for further development. We now propose further mechanistic studies and chemical modifications of these compounds in efforts to 1) determine how they kill myeloma cells, 2) optimize their effects, and 3) advance their development toward intended eventual human anti-myeloma clinical trials.

Targeting the SCF/skp2 pathway for the treatment of multiple myeloma
Year Awarded: 2006 Type of Grant: Research Fellow Awards
Location: United States Institution: The University of North Carolina at Chapel Hill
Amount: $75,000 Investigator: Qing Chen
The cyclin-dependent kinase inhibitor p27(Kip1) is a critical cell cycle regulator, and decreased p27 levels are associated with poor prognosis in a variety of malignancies, including multiple myeloma. Decreased p27Kip1 expression occurs primarily through enhanced proteolysis by up-regulation of the SCF(Skp2)-Cks1 E3 complex responsible for p27 ubiquitination. We hypothesize that, unlike proteasome inhibition, targeting SCF(Skp2) will provide a more specific means of activating programmed cell death without induction of anti-apoptotic pathways. Based on encouraging preliminary data, we propose additional studies using genetic and pharmacologic approaches to validate SCF(Skp2 ) as a novel, rational target for myeloma therapy.

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