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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.

Pre-clinical validation of IL-6 for translational myeloma research
Year Awarded: 2009 Type of Grant: Senior Research Awards
Location: United States Institution: The University of Iowa
Amount: $200,000 Investigator: Siegfried Janz
The involvement of interleukin-6 (IL-6) in the growth, proliferation, and survival of myeloma cells has engendered considerable interest in targeting IL-6 in MM patients for therapeutic purposes. However, the promise of IL-6 as a target for novel antibody- and small molecule-based myeloma therapies has not yet been translated into clinical benefits for myeloma patients. The research proposed here seeks to address fundamental outstanding questions on the role of IL-6 in the natural history of multiple myeloma in order to facilitate, from the preclinical perspective of a cancer biologist, the ongoing effort of the pharmaceutical industry to target IL-6 more effectively.

Effects of IMiDs on granulocytic maturation
Year Awarded: 2009 Type of Grant: Senior Research Awards
Location: United States Institution: University of Pittsburgh
Amount: $200,000 Investigator: Suzanne Lentzsch
IMiDs can induce low white blood cells (WBC) and blood clots, which can be fatal. We showed that IMiDs block maturation of WBC resulting in low WBC in the blood and accumulation in the bone marrow. Elevated numbers of immature WBC produce more Cathepsin G (CG) increasing the risk of clots since CG is a potent stimulator of platelet aggregation. We will evaluate the connection between low WBC and blood clots due to blocking maturation of WBC. We will also analyze whether overcoming the maturational arrest by growth factors and subsequent maturation of WBC will reduce the risk for clots.

Multiple Myeloma Therapeutics Based on the Natural HDACi Largazole
Year Awarded: 2009 Type of Grant: Senior Research Awards
Location: United States Institution: Colorado State University
Amount: $200,000 Investigator: Robert Williams
The purpose of this application is to develop new drug classes that target a new and exciting biochemical target recently recognized as being essential to the cancer cell cycle. The new class of enzymes that exist inside cells called histone deacetylase enzymes (HDAC��_s). Our multidisciplinary project brings together synthetic organic chemistry, computational modeling, chemical biology and clinical evaluation of potential inhibitors of HDAC��_s. As members of this family of agents have shown considerable promise in human clinical trials to treat multiple myeloma, especially FK228 (Romidepsin), we plan to develop more potent, selective and less toxic drugs within this structural family.

Harnessing anti-SOX2 T cells in myeloma: preclinical studies
Year Awarded: 2009 Type of Grant: Senior Research Awards
Location: United States Institution: Yale University
Amount: $200,000 Investigator: Madhav Dhodapkar
Current therapies lead to high rates of disease remission in myeloma, but nontoxic approaches to prevent recurrence are needed. Although the immune system has a capacity to control tumors, the nature of targets of protective immunity remain unknown. Recently we have shown that immune response against an antigen SOX2, which is critical for biology of embryonal stem cells and also expressed on a subpopulation of tumor cells, predicts exceptionally good outcome in myeloma. The goal of these studies is to better understand how to boost activation of such responses as a first step towards harnessing these responses in patients.

p62 Signaling as a Therapeutic Target for Multiple Myeloma
Year Awarded: 2009 Type of Grant: Senior Research Awards
Location: United States Institution: University of Pittsburgh
Amount: $200,000 Investigator: Noriyoshi Kurihara
The bone microenvironment plays a critical role in the growth of myeloma (MM) cells and the bone destruction caused by MM. We recently found that p62 is a protein that is involved in multiple signaling pathways that increase tumor growth and osteoclast formation in MM patients. Further, decreasing p62 levels in the marrow microenvironment decreases the growth of MM cells and osteoclast formation. In this proposal, we will identify the parts of p62 involved in increasing MM cell growth and bone destruction and use these results to develop new agents to treat MM.

GFI-1 Suppression of Osteoblast Differentiation in Myeloma
Year Awarded: 2009 Type of Grant: Senior Research Awards
Location: United States Institution: University of Pittsburgh
Amount: $200,000 Investigator: G. David Roodman
Bone formation is markedly decreased in myeloma, and the cause is unknown. We will identify and characterize the factors produced and induced by myeloma cells in bone cells that decrease the development of bone forming cells in the marrow. We will use the results of these studies to develop potential new treatments for myeloma.

Investigating the Anti-Myeloma Effects of Clioquinol
Year Awarded: 2009 Type of Grant: Research Fellow Awards
Location: International Institution: University Health Network
Amount: $75,000 Investigator: Mahadeo Sukhai
The proteasome is an enzymatic complex that degrades excess and misfolded proteins in the cell. The off-patent antimicrobial, Clioquinol, was identified to inhibit the proteasome and induce cell death in malignant cells through a copper-dependent mechanism. Here, we will examine how Clioquinol and copper inhibit the proteasome and test the hypothesis that they act through a previously unknown mechanism. We will undertake an early stage clinical trial of oral Clioquinol in patients with refractory leukemia. This work is highly translational as we strive to repurpose Clioquinol as an anti-cancer agent and advance a molecule from our laboratory to clinical trial.

Validation of withaferin A as an anti-myeloma compound
Year Awarded: 2008 Type of Grant: Validation of Novel Compounds and Combinations
Location: International Institution: Universiteit Gent
Amount: $199,088 Investigator: Wim Vanden Berghe
Withania somnifera (ashwagandha) has been used for centuries in traditional Ayurvedian medicine to treat inflammation and cancer. Several studies have shown that Withaferin A (WA) is the most potent anti-cancer compound present in Withania leaf extracts. Although we found that WA blocks several cell survival mechanisms in lymphoma and multiple myeloma, the clinical usefulness of WA for MM treatment has never been investigated. Therefore, in the proposed study, we would like to investigate whether 1) WA kills MM cells, but not normal blood cells, from patients with MM and 2) WA can inhibit disease progression in a MM mouse model.

Targeting Deubiquitylase enzyme USP-7 as Therapy in 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: Dharminder Chauhan
The normal cell functioning requires elimination of unwanted proteins from cells, and this process is mediated by the Ubiquitin-Proteasome System (UPS). Blockade of UPS causes accumulation of unneeded proteins and cell death. Cancer cells are more sensitive to UPS inhibition than normal cells, since their rate of protein degradation is higher. This notion led to the development of first-in-class proteasome inhibitor bortezomib as a cancer therapy. In the proposed study, I will examine the effects of another newly developed drug called P5091, which blocks protein breakdown to provide the framework for clinical trials in multiple myeloma.

Inhibition of the autophagic survival response to enhance chemotherapy
Year Awarded: 2008 Type of Grant: Validation of Novel Compounds and Combinations
Location: United States Institution: University of Arizona
Amount: $200,000 Investigator: Terry Landowski
Changes in Ca2+ regulate a range of critical cell processes, including metabolic activity, cellular stress response and programmed cell death. Our recent work indicates that ER stress induced apoptosis, initiated by clinically active proteasome inhibitors, is dependent on the modulation of mitochondrial function by Ca2+. This proposal is designed to investigate the relationship between mitochondrial Ca2+ regulation and mitochondrial-mediated apoptosis in the ER stress response. The central hypothesis to be tested is that ER stress activated apoptosis is modulated by specific changes in mitochondrial signaling and function. When mitochondrial Ca2+ signaling is restricted, an autophagic survival response is initiated (specific aim 1). Inhibition of the autophagic survival response will promote the therapeutic index of agents that induce ER stress (specific aim 2). Thus, targets for therapeutic intervention exist at several sites including regulating mitochondrial metabolism and the binding properties of several purported regulators of mitochondrial permeability. Furthermore, the mechanistic studies proposed here have implications for potential strategies with other clinical agents known to activate stress and autophagy pathways.

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