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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.

Comparative oncogenomic to identify myeloma progression events
Year Awarded: 2008 Type of Grant: Senior Research Awards
Location: United States Institution: Mayo Clinic Arizona
Amount: $200,000 Investigator: Marta Chesi
Genetically engineered mice can provide unique insights critical to understanding tumor biology. They can be used to validate the role of genes found mutated in cancer. Also, they provide a great preclinical tool to test drug efficacy against tumor specific targets. Here we propose to interrogate the entire genome of our myeloma prone mice to identify mutations (genomic amplifications or deletions) that cause rapid growth of the myeloma cells. Candidate gene will then be inserted in the genome of our myeloma prone mice to validate their contribution to tumor progression. We expect the identification of these genes in the mouse will give us novel clues to pathways important in human myeloma tumorigenesis.

Targeting Wnt Signaling in Myeloma Using Stabilized Alpha-Helices of BCL9
Year Awarded: 2008 Type of Grant: Senior Research Awards
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $200,000 Investigator: Ruben Carrasco
Multiple Myeloma (MM) is a cancer involving cells that normally comprise a small population in the bone marrow. In this disease, however, certain changes in the genetic information of the cells cause them to multiply in number and become malignant. In our previous studies we have identified a genetic abnormality involving the Wnt signaling pathway that may be responsible for the disease progression. We have identified one such abnormality in many patients pointing to aberrant cellular processes responsible for the ability of the cancer cells to spread within and beyond the bone marrow microenvironment. We would like to develop short peptides to block the interaction between BCL9 and ��_��_-catenin, a critical event for the activation of the Wnt pathway. We will validate these peptides in mice with the intent of developing therapies for future use in patients.

Beta 1 integrin inhibitory peptides: Novel agents for the treatment of MM
Year Awarded: 2008 Type of Grant: Senior Research Awards
Location: United States Institution: H. Lee Moffitt Cancer Center and Research Institute
Amount: $200,000 Investigator: Lori Hazlehurst
Our laboratory previously showed that �_�1 integrin mediated signaling can confer drug resistance. In this proposal we provide preliminary data that �_�1 integrin inhibitory peptide referred to as HYD1 has anti-tumor activity as a single agent in vitro and in vivo. Furthermore the mechanism of cell death is independent of the activation of downstream caspases. The goals of this proposal are a) to delineate the mechanism of HYD1 induced cell death and b) determine optimal combination strategies for HYD1 treatment in multiple myeloma in vtro and in vivo.

Anti-b2M monoclonal antibodies as therapeutic agent for myeloma
Year Awarded: 2008 Type of Grant: Senior Research Awards
Location: United States Institution: University of Texas M.D. Anderson Cancer Center
Amount: $200,000 Investigator: Qing Yi
b2-microglobulin (b2M) is a small protein molecule found in the blood of healthy individuals. However, in myeloma patients, levels of b2M are highly elevated in the blood. We found that anti-b2M antibodies, made by the immune system against b2M, killed more than 70% of tumor but not normal blood cells. To examine whether these anti-b2M��_n antibodies may be used to treat patients with myeloma, we will determine how they are able to kill tumor cells, and whether they kill also normal blood cells. Finally, we will study if combining anti-b2M��_nantibodies with chemotherapy drugs kills more tumor cells.

From laboratory to clinic; Dimethylaminoparthenolide (DMAPT) in myeloma
Year Awarded: 2007 Type of Grant: Validation of Novel Compounds
Location: United States Institution: Indiana University (Indianapolis)
Amount: $100,000 Investigator: Attaya Suvannasankha
Nuclear factor kappa B (NFkB) is a pathway that promotes growth of multiple myeloma (MM) cells and makes them resist to cancer drugs. Parthenolide, an herbal derivative, is very active against NFkB and attacks both multiple myeloma cells and their supportive cells in the bone marrow. However parthenolide is poorly absorbed. We propose to study Dimethylaminoparthenolide (DMAPT), a modified parthenolide molecule, that is absorbed easily and gives high blood levels of parthenolide in animals. We will test the ability of DMAPT in mice that have been transplanted with MM cells, alone and together with other MM drugs.

A combination strategy targeting the Bcl-2 family in multiple myeloma
Year Awarded: 2007 Type of Grant: Validation of Novel Compounds
Location: United States Institution: Virginia Commonwealth University
Amount: $100,000 Investigator: Steven Grant
Recent studies from our laboratory have shown that a clinically relevant cell cycle inhibitor (flavopiridol) dramatically increases the anti-myeloma activity of a novel cell death inducer (GX15-070) in multiple myeloma (MM) cells. We propose to optimize this regimen in MM cells, investigate the mechanisms responsible for synegism, determine whether the regimen is selective for MM cells and overcomes drug resistance, and is effective in an animal model of MM. It is anticipated that these studies will lead to the development of novel therapeutic protocol employing a new flavopiridol schedule in combination with GX15-070 in patients with MM.

Combining IGF-1R and HDAC inhibitors in MM models in vitro and in vivo
Year Awarded: 2007 Type of Grant: Validation of Novel Compounds
Location: International Institution: Vrije Universiteit Brussel
Amount: $100,000 Investigator: Karin Vanderkerken
Multiple myeloma (MM) is a deadly plasma cell cancer that resides in the bone marrow where the tumor cells are provided with necessary growth signals. IGF-1 is one of the key growth signals. We have previously shown that targeting IGF-1 by picropodophyllin (PPP) represents an attractive therapeutic strategy. Although non-toxic for the patient and highly specific for the target, resistance to all drugs will develop. To overcome resistance and enhance the sensitivity of PPP in MM, we therefore performed a screen for combinatorial drug candidates. In this approach we address the possibility that combinations of PPP with one of these candidates, the HDAC inhibitor LBH 589 will prove useful in combinatorial management of MM.

Delineation of differential role of canonical & non-canonical NF-kB pathway
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $200,000 Investigator: Teru Hideshima
Nuclear factor (NF)-kB is a transcription factor mediating expression of various proteins which play crucial roles in multiple myeloma (MM) cell growth and drug resistance, adhesion to bone marrow stromal cells (BMSCs), and cytokine secretion in BMSCs. NF-kB signaling is dissected into classical (canonical) and alternative (non-canonical) cascades. I will examine molecular mechanisms as well as downstream target proteins and biologic sequelae of each cascade in MM. I will then delineate the effects of blockade of canonical and/or non-canonical NF-kB signaling on growth of MM cells in the BM milieu, to provide the framework for derived clinical trials.

The Role of NFkB Pathway Mutations in Multiple Myeloma
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: Mayo Clinic Arizona
Amount: $200,000 Investigator: Leif Bergsagel
Multiple myeloma is an incurable cancer that results from the accumulation of several genetic mutations. These mutations uniquely distinguish the cancer cells from normal cells, and it is believed that tumor cells become addicted to the pathways activated by these mutations. As a result they represent a tumor specific vulnerability that can be exploited therapeutically using drugs that target the pathways activated by mutation. We have recently identified mutations in myeloma cells that activate one of the most fundamental pathways in immunology, called the NFkB pathway. We now propose to study the functional consequence of these mutations.

Validation of an Anti-JAG2 MAb for Treatment of Multiple Myeloma
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: Health Research Incorporated, Roswell Park Cancer Institute Division
Amount: $200,000 Investigator: Lionel Coignet
We have shown that the NOTCH pathway is essential for the survival and proliferation of the malignant plasma cells and that a ligand for this pathway, JAG2, is over-expressed in myeloma cells. This is of particular importance since it controls secretion of critical cytokines from the stromal cells, such as IL6, VEGF and IGF-1. In this proposal, we will determine whether blocking activation of NOTCH pathway with a proprietary anti-JAG2 monoclonal antibody increases the efficacy of bortezomib and prevents chemoresistance 1) in cellular, as well as 2) in mouse models.

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