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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.

Identifying therapeutic targets for FGFR3-associated MM
Year Awarded: 2006 Type of Grant: Senior Research Awards
Location: United States Institution: The Regents of the University of California
Amount: $200,000 Investigator: Leslie Thompson
In many MM cases, there is increased activity of fibroblast growth factor receptor 3 (FGFR3), which is associated with a poor prognosis. Increased FGFR3 activity promotes cancer growth and resistance to chemotherapy. We will determine if FGFR3 also alters the proteins outside of the MM cells contributing to its spread. We will test a new therapeutic approach that may interrupt many of the effects of FGFR3. In addition, using a novel yeast system, we will screen drugs and identify other components of the FGFR3 system that would be targets for future therapies.

Treatment of Multiple Myeloma with a humanized mononclonal antibody
Year Awarded: 2006 Type of Grant: Senior Research Awards
Location: United States Institution: Temple University- HSC
Amount: $100,000 Investigator: Robert Colman
Multiple myeloma, produces proteins related to the immune system which results in kidney disease, bone destruction and decreased red blood cell number. We have developed a mouse antibody specific to a human blood protein, kininogen. Which antibody can decrease the growth of mouse myeloma cells, by preventing the formation of new blood vessels. We will reconstruct the mouse antibody to resemble a human antibody and determine how well the humanized antibody works against both mouse and human multiple myeloma. We will to determine the best doses and treatment schedules for the humanized antibody in mice and translate these to patients.

Adoptive immunotherapy with donor myeloma-specific T cells
Year Awarded: 2006 Type of Grant: Senior Research Awards
Location: United States Institution: University of Texas M.D. Anderson Cancer Center
Amount: $100,000 Investigator: Larry Kwak
The overall goal of our proposal is to develop therapy for patients with multiple myeloma. We combine a vaccine strategy with stem cell transplantation from healthy donors. These tumor cells express a tumor-specific antigen termed ��_idiotype.��_ Healthy donors are immunized with this protein, activating immune cells that can recognize and eliminate tumor cells when transplanted into myeloma patients. We propose testing whether immunity against the idiotype protein can be transferred from donor to recipient. We will also characterize the immune cells engineered to kill tumor cells. Collectively, these studies will enable us to optimize therapy for multiple myeloma.

Synergy of Aplidin and LBH589 with conventional anti-myeloma treatments
Year Awarded: 2006 Type of Grant: Validation of Novel Compounds
Location: United States Institution: Centro de Investigacion del Cancer
Amount: $100,000 Investigator: Atanasio Pandiella
Multiple myeloma (MM) is a B cell malignancy characterized by the accumulation of plasma cells and the production of immunoglobulins. Although important progress has been achieved in the treatment of this disease, curative treatments are still unavailable. Therefore it is necessary to develop new treatments in order to eradicate the disease. Usually, active treatments for hematological malignancies are based on combinations of several drugs (three or four) with different mechanisms of action. Although some novel drugs, such as bortezomib or the immunomodulatory compounds, have shown clear activity in MM, most patients relapse. This illustrates the need for investigating appropriate drug combinations in order to overcome drug resistance. The above facts clearly call for attempts to improve MM treatment by the use of combinations of drugs that act through different mechanisms. We have extended experience with two compounds, LBH589 and Aplidin, which target different routes with respect to conventional treatments. We intend o analyze whether Aplidin and LBH589 can potentiate the conventional anti-myeloma treatments.

Multi-Targeted Kinase Inhibition-Based Combination Strategies in Myeloma
Year Awarded: 2006 Type of Grant: Validation of Novel Compounds
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $100,000 Investigator: Constantine Mitsiades
Our recent studies have shown that the growth of myeloma cells can be triggered by multiple kinase molecules. These diverse targets can be simultaneously blocked with inhibitors of hsp90, a protein which facilitates the function of many such important kinases, or with multi-targeted kinase inhibitors, i.e. inhibitors which can simultaneously block the active portion of many different kinases. We have observed that hsp90 inhibitors and multi-targeted kinase inhibitors can be safely administered in animal models of myeloma and achieve anti-tumor responses. In this project, we will define the role of these agents administered in combination treatments with other promising investigational anti-myeloma treatments, aiming at enhancing their anti-myeloma activity, with the ultimate goal of improving the outcome of patients with myeloma.

Combined Therapy Of Bortezomib And BMS-345541 In A Myeloma Mouse Model
Year Awarded: 2006 Type of Grant: Validation of Novel Compounds
Location: United States Institution: H. Lee Moffitt Cancer Center and Research Institute
Amount: $99,936 Investigator: Zhi-Wei Li
Multiple Myeloma is an incurable blood cancer representing approximately 2% of all cancer deaths. Recently, FDA approved Bortezomib for the treatment of patients with relapsed myeloma. Bortezomib has several putative targets including the transcription factor NF-kB. We have found that blocking NF-kB activation increased sensitivity of myeloma cells to Bortezomib cytotoxicity. In this project, we propose to validate this finding using a myeloma mouse model. Our work will provide an important pre-clinical in vivo evidence for the development of a new therapeutic modality involving a combined regimen of BMS-345541, an NF-kB inhibitor, and Bortezomib in multiple myeloma therapy.

Role of SLRPs in the anti-myeloma response of osteoblasts
Year Awarded: 2006 Type of Grant: Senior Research Awards
Location: United States Institution: University of Arkansas
Amount: $99,759 Investigator: Shmuel Yaccoby
Our goal is to develop interventions to simultaneously control myeloma and the accompanying painful bone disease. We showed that bone-forming cells (osteoblasts) inhibit myeloma growth. Osteoblasts produce high levels of small leucine-rich proteoglycans (SLRPs), some of which suppress tumor growth. We propose the following studies: (Aim 1) Determine the involvement of SLRPs in osteoblast-induced myeloma growth inhibition and test their anti-myeloma efficacy in our animal model; (Aim 2) Determine the effects of potent osteoblast-activating agents on bone formation and myeloma development and progression in our animal model. This study will develop alternative, safe approaches for controlling myeloma progression.

Combination Therapies Targeting Proteasome, Mitochondria and NF-kappa B
Year Awarded: 2006 Type of Grant: Validation of Novel Compounds
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $100,000 Investigator: Dharminder Chauhan
Multiple Myeloma (MM) remains fatal despite all available therapies. Novel approaches that simultaneously target cellular mechanisms regulating growth and conferring chemoresistance in MM cells are needed. My studies have identified various novel treatments that target distinct components within the MM cells such as proteasomes (regulates protein degradation) or mitochondria (regulates cell respiration); therapeutic strategies combining these novels agents will block cell growth and increase cell death. Although individual agents show independent anti-MM activity, combinations of agents will be necessary to enhance cytotoxicity, abrogate drug resistance, and ultimately improve patient outcome.

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.

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