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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 Combination Therapies for Mutiple Myeloma
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: The University of Alabama at Birmingham
Amount: $200,000 Investigator: Yang Yang
General Audience Abstract: Briefly describe your proposed project in 100 words or less. Be sure to use language that can be easily understood by a general audience. Current anti-myeloma drugs can not kill all tumor cells. Heparanase is an enzyme that rarely exists in normal tissue but is preferentially expressed in human tumors including multiple myeloma (MM). Our previous experiments demonstrated that heparanase promotes growth and metastasis of MM ; and a heparanase inhibitor, 100NA,RO-H dramatically suppresses myeloma tumor growth in animal models of MM . Because 100NA,RO-H targets different mechanism of tumor growth, compare to current anti-myeloma drugs, we will investigate, in present study, if adding 100NA,RO-H to clinic anti-myeloma drugs can more effectively kill tumor cells and improve MM patients��_ survival in the future.

Cell cycle based combination therapy for multiple myeloma
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: Joan and Sanford I. Weill Medical College of Cornell University
Amount: $200,000 Investigator: Selina Chen-Kiang
Myeloma is treatable but incurable because current therapies can��_t successfully control cancer cell division. We have identified two novel therapeutic targets that promote cancer cell division, Cdk4 and Cdk6, and demonstrated that they are completely inhibited in patient myeloma cells by PD 0332991, an orally bioactive small molecule. PD 0332991 also prevents human myeloma tumor growth in animal models, and strikingly enhances the killing of myeloma cells by other therapies. A randomized Phase I/II clinical trial for PD 03332991-Velcade will soon be initiated. This work will complement the trial and advance the development of PD 0332991-based combination therapy.

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.

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