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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.

The activity of novel PI3K inhibitors in myeloma
Year Awarded: 2008 Type of Grant: Validation of Novel Compounds and Combinations
Location: International Institution: Institute of Cancer, Barts and the London School of Medicine, Queen Mary University of London
Amount: $199,984 Investigator: Simon Joel
Myeloma is a bone marrow cancer involving cells that fight infection. The average survival for new patients is only 4 years, suggesting new treatments are urgently required. Myelomas are particularly dependent on a pathway that signals from the cell surface to the nucleus. We plan to study the activity of novel, potent inhibitors of a specific protein in this pathway. The effect of these agents on cell growth and viability will be studied when used alone, and when combined with established anti-myeloma drugs. Importantly we intend to use novel methods for measuring the effect of these drugs on pathway signaling.

Targeting the MUC1 Oncoprotein in Multiple Myeloma
Year Awarded: 2008 Type of Grant: Validation of Novel Compounds and Combinations
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $200,000 Investigator: Donald Kufe
The MUC1 protein is expressed at high levels in cells from patients with multiple myeloma. Recent work has shown that MUC1 contributes to the growth and survival of multiple myeloma cells. However, there are presently no drugs to block MUC1 in the treatment of multiple myeloma. The proposed work will focus on the development of peptide drugs that inhibit MUC1 function. The drugs will be tested in the laboratory and in animal models of multiple myeloma. The results obtained will be used to further develop these agents for the treatment of patients with multiple myeloma.

RAP-011, A Novel Activin Antagonist in the Treatment of Myeloma
Year Awarded: 2008 Type of Grant: Validation of Novel Compounds and Combinations
Location: United States Institution: Massachusetts General Hospital (The General Hospital Corp.)
Amount: $200,000 Investigator: Noopur Raje
Multiple myeloma (MM) is often complicated by severe bone disease. RAP-011 is a novel compound that effectively stimulates bone formation in animal models of osteoporosis. In this project we will study the effects of RAP-011 on bone disease in the context of MM. Our preliminary data suggests that RAP-011 induces bone formation, while inhibiting resorption. Indirect anti-MM effects are also noted. We will combine RAP011 with catabolic agents such as bisphosphonates with the goal of restoring bone homeostasis in MM. These studies will provide the basis for future clinical development of bone-anabolic agents in MM.

Validation of pyrimidinetriones as potential therapy for multiple myeloma
Year Awarded: 2008 Type of Grant: Validation of Novel Compounds and Combinations
Location: United States Institution: Joan and Sanford I. Weill Medical College of Cornell University
Amount: $200,000 Investigator: Hsiou-Chi Liou
Despite available therapies, multiple myeloma remains fatal, as drug toxicity and drug resistance ultimately develops. The Rel/NF-kB family of transcription factors (TFs) plays an important role in myeloma cell growth, survival, drug resistance, and migration and is considered therapeutic targets for MM. This project focuses on developing Rel-member-specific small molecular inhibitors as novel therapies for MM. We have initiated a drug discovery program, and thus far identified several classes of candidate compounds that target the classical Rel pathway. Here, we propose to optimize and validate one class of lead compounds as potential drug candidates for multiple myeloma.

TH17 cytokines in myeloma: Immunotherapeutic targets
Year Awarded: 2008 Type of Grant: Research Fellow Awards
Location: United States Institution: Boston VA Research Institute, Inc.
Amount: $75,000 Investigator: Rao Prabhala
With all the therapeutic advances, for the most part, myeloma remains incurable. This has prompted innovative investigations including role of immune mechanism in myeloma progression as well as therapeutic applications of immunotherapy. We have preliminary results suggesting elevated levels of pro-inflammatory cytokines and immune cells in myeloma. In this application our main goal is to characterize the role of pro-inflammatory cytokines that are known to be part of myeloma bone marrow microenvironment and how they are helping the progression of myeloma as well as protect them from immune mediated killing. We will identify their role in myeloma growth and survival to then develop therapeutic strategies targeting these pro-inflammatory cytokines

Tissue-Based Array Classification of Multiple Myeloma
Year Awarded: 2008 Type of Grant: Research Fellow Awards
Location: United States Institution: The University of Calgary
Amount: $75,000 Investigator: Alex Klimowicz
Stem cell transplantation (SCT) is the cornerstone treatment for multiple myeloma, however not all patients benefit from such approach. There are currently no practical or easily reproducible model to predict ahead of time who would not benefit from such aggressive therapeutic approach. We are developing a tissue array method to help us classify myeloma patients into different subgroups and ideally allow us to predict accurately whether or not they are good candidate from SCT. Once implemented this approach can help spare many patients unnecessary toxicities and perhaps guide them for better ��_tailored��_ therapy.

Epigenetic Deregulation by The Multiple Myeloma SET Domain Protein
Year Awarded: 2008 Type of Grant: Research Fellow Awards
Location: United States Institution: Northwestern University - Chicago Campus
Amount: $75,000 Investigator: Eva Martinez
In the past decade it was discovered that multiple myeloma cells harbor shuffled, rearranged genes. This may lead to changes in gene function and the development of the disease. We are studying one such gene, MMSET. The MMSET gene makes a protein that in turn represses other genes in the cell. An overabundance of MMSET in myeloma cells may lead to an abnormal shutdown of target genes and disease development. We will use biochemical techniques to prove this hypothesis and identify the genes and pathways disrupted by MMSET. Such pathways might represent new therapeutic targets in myeloma.

The Role of Selectins in Multiple Myeloma
Year Awarded: 2008 Type of Grant: Research Fellow Awards
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $75,000 Investigator: Abdel Kareem Azab
Multiple-Myeloma is characterized by its spread to different sites in the bone-marrow, involving cell-translocation from the bone-marrow to the blood-stream and reentry back to the bone-marrow. Selectins are molecules that play a major role in the mechanism of entry of white-blood-cells through blood-vessels��_-walls to target tissues such as lymph-nodes and inflammation-sites. However, their role in multiple-myeloma has not been explored. In this proposal, we will investigate the role of selectins in the spread of multiple-myeloma cells to the bone-marrow, and the potential therapeutic benefit of neutralizing their activity with drugs to prevent multiple-myeloma propagation and spread in animal models.

Heparanase as a target for myeloma treatment
Year Awarded: 2008 Type of Grant: Research Fellow Awards
Location: International Institution: Hadassah Medical Organization
Amount: $75,000 Investigator: Eyal Zcharia
The heparan sulfate degrading enzyme, heparanase, promotes myeloma growth and metastasis. Heparanase expression correlates with increased tumor vascularity and myeloma bone metastasis, indicating that the enzyme is an important target for drug development. Our recent data indicate that a newly developed inhibitor of heparanase enzymatic activity inhibits myeloma growth and metastasis in mice. Yet, non enzymatic activities, exerted by specific domains of the heparanase protein, contribute to tumor growth, survival and metastasis. We propose to generate inhibitors against non-enzymatic functions of heparanase that in combination with the existing enzyme inhibitor and/or the currently available treatments, will better suppress myeloma progression.

Evaluation of p97 as a Potential Target in Multiple Myeloma
Year Awarded: 2008 Type of Grant: Research Fellow Awards
Location: United States Institution: California Institute of Technology
Amount: $75,000 Investigator: Tsui-Fen Chou
The ubiquitin��_proteasome system (UPS) tags proteins with ubiquitins, which target them to the proteasome for degradation. The FDA��_s approval of the proteasome inhibitor, bortezomib, for treatment of multiple myeloma has inspired broad interest in developing drugs against other UPS components. p97 helps deliver ubiquitin-tagged proteins to the proteasome. It is an intriguing drug target because it is over-expressed in cancers, and is implicated in turnover of proteasome substrates that are thought to be crucial for cancer cell survival. We propose to employ a combination of a proteomic screening and medicinal chemistry to identify substrates and inhibitors of p97.

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