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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.

PARP inhibitor as novel therapeutic approach in Multiple Myeloma
Year Awarded: 2010 Type of Grant: Research Fellow Awards
Location: International Institution: The University of Calgary
Amount: $75,000 Investigator: Ernesta Paola Neri
The proteasome inhibitor Bortezomib has significantly improved the outcomes of myeloma (MM) patients. However nearly all patients eventually acquire resistance to its effects. We have identified a novel therapeutic approach that takes advantage of the unstable genome in MM cells by altering their ability to maintain their DNA integrity. Combining a PARP inhibitor that promotes DNA breakage within the tumoral cells with Bortezomib, which inhibits the DNA repair machinery results in catastrophic DNA damages that are lethal to MM cells. Therefore inhibition of PARP in the presence of proteasome inhibitors might have just uncovered the Achilles��_ heel of MM cells.

The NFKB2-IL10 Pathway in Multiple Myeloma Pathogenesis
Year Awarded: 2010 Type of Grant: Research Fellow Awards
Location: United States Institution: Medical College of Georgia Research Institute, Inc.
Amount: $75,000 Investigator: Brian McCarthy
Multiple Myeloma (MM) is a common cancer of the immune system considered incurable despite major advances. Much is known about specific genes involved in MM development. However, the relationships between critical genes, important signaling pathways and their influence on outcome and survival are unclear. Evidence is increasing to support important roles for persistent NF-B2 signaling and mutations in the NF-B2 gene. This project seeks to examine a possible link between NF-B2 and IL-10, a protein produced by many myeloma cells. Therapeutic intervention by blocking IL-10��_s signal in patients with NF-B2 mutations may provide an important new weapon against MM.

The role of survival proteins in multiple myeloma development
Year Awarded: 2010 Type of Grant: Research Fellow Awards
Location: International Institution: The Walter and Eliza Hall Institute of Medical Research
Amount: $75,000 Investigator: Victor Peperzak
Multiple myeloma (MM), also known as Kahler��_s disease, is a cancer of plasma cells. MM is the second most prevalent blood cancer (10%) after non-Hodgkin��_s lymphoma and manifests systemic symptoms that make it difficult to diagnose. While the underlying mechanism of MM development remains unclear, the persistence of MM cells seems to depend highly on certain survival molecules. By making use of different mouse models we can study the specific contribution of these survival molecules for the development of MM. These findings will enhance our understanding of MM cell survival and may therefore prove instrumental for the treatment of MM.

Targeting UBC13 for Multiple Myeloma Treatment
Year Awarded: 2010 Type of Grant: Research Fellow Awards
Location: United States Institution: Burnham Institute for Medical Research
Amount: $75,000 Investigator: Charitha Madiraju
Multiple myeloma (MM) is a cancer of the bone marrow caused due to overgrowth of white blood cells. While most of the existing medications have toxicity issues, there is no cure for the disease. Thus, a need exists for treating relapsed and refractory MM with novel medicines that might help provide long-term remission. In this proposal, we seek to investigate chemicals that neutralize UBC13-UEV1A, a critical signaling molecule that operates downstream of cancer-promoting pathways implicated in MM. We will examine whether these chemicals can suppress cancer cell activity in the laboratory and ameliorate disease in a mouse model of MM.

Measuring the apoptotic preset as a predictor of chemosensitivity
Year Awarded: 2010 Type of Grant: Research Fellow Awards
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $75,000 Investigator: Triona Ni Chonghaile
When chemotherapy kills multiple myeloma cells, it does so by triggering a program in the cancer cell that forces the cancer cell to commit suicide. Unfortunately, chemotherapy often does not succeed in eradicating cancer cells. My hypothesis is that the way these cancer cells escape is by rendering themselves resistant to this cell suicide program. I will make use of a novel tool on myeloma samples from actual patients to test whether this is indeed the case. If so, we can then begin to dismantle the blocks in the suicide program to render resistant myeloma cells sensitive once again to chemotherapy.

Macrophages protect myeloma cells from chemotherapy drug-induced apoptosis
Year Awarded: 2010 Type of Grant: Research Fellow Awards
Location: United States Institution: University of Texas M.D. Anderson Cancer Center
Amount: $75,000 Investigator: Yuhuan Zheng
Multiple myeloma is the most common type of bone malignancy in the United States. These patients have an accumulation of tumor cells in their bone marrow. Chemotherapy is the most effective treatment for the disease. However, myeloma cells develop drug resistance within the bone marrow, resulting in treatment failure and patient death. For the first time, our lab has shown that bone marrow macrophages interact with myeloma cells and promote myeloma drug resistance. Here we propose mechanistic studies to demonstrate the role of macrophages in myeloma drug resistance. Results from our work may improve current chemotherapy treatments for the disease.

An Integrated Study of Proteostasis Against Multiple Myeloma
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: International Institution: Fondazione Centro San Raffaele del Monte Tabor
Amount: $200,000 Investigator: Simone Cenci
Novel therapies are demonstrating that protein degradation can be targeted to combat Multiple Myeloma, a still incurable cancer. However, our poor understanding of proteasomes and autophagy, the main machineries that protect the cell from accumulation of unwanted proteins, is a major limitation. Our research plan aims to identify informative markers and innovative molecular targets against Multiple Myeloma by investigating the mechanisms regulating proteasome function, autophagy, and their cross-talk. To achieve this goal, we will deploy a powerful multidisciplinary platform integrating molecular biology, bioinformatics, functional genomics, and cellular imaging technologies.

Targeting type 1 IFN and TRAIL to MM using anti-CD138 fusion proteins
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: United States Institution: The Regents of the University of California
Amount: $200,000 Investigator: Sherie Morrison
Type 1 interferons, molecules capable of killing cancer cells, have long been used for the treatment of multiple myeloma (MM). However, to date their efficacy has been limited in part because of their toxicity. TRAIL is another molecule that can kill cancer cells. CD138 is a protein present on the surface of MM cells and antibodies specific for CD138 will bind to MM cells. We propose to produce recombinant proteins in which in interferon or TRAIL is genetically linked to anti-CD138. These proteins should bind to MM cells making both interferon and TRAIL more potent in killing MM cells.

Novel Treatment Approaches to Target the RARa2 Positive Myeloma Cell
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: United States Institution: University of Utah
Amount: $200,000 Investigator: Fenghuang Zhan
Multiple myeloma remains largely incurable. We recently found that tumor cells from about 30% of patients with myeloma express the RARa2 gene. Such patients had a shorter survival. Interestingly, ATRA, a vitamin A derivative that has been very successful in the treatment of acute promyelocytic leukemia, selectively kills myeloma cells expressing RARa2, but not those without RARa2 expression. Furthermore, ATRA-induced anti-myeloma activities were associated with down-regulation of Wnt/ beta-catenin signaling pathway, which is important for rapid tumor growth. Therefore, we propose preclinical research to exploit new approaches based on the combination of ATRA and Wnt signal targeting drugs to treat RARa2-positive myeloma.

Mechanisms of Lenalidomide Resistance
Year Awarded: 2010 Type of Grant: Senior Research Awards
Location: United States Institution: University of Texas M.D. Anderson Cancer Center
Amount: $200,000 Investigator: Robert Orlowski
Lenalidomide (Revlimid�_�) is one of our best anti-myeloma drugs, and is used in the newly diagnosed, maintenance, and relapsed/refractory settings. Unfortunately, myeloma cells eventually develop drug resistance through as yet poorly understood mechanisms. We have developed novel models of lenalidomide resistance to study this phenomenon, and already used them to identify some of the pathways involved. Additional studies are proposed to further validate the role of these pathways, and to test approaches to suppress them. These will be translated to the clinic to both increase the effectiveness of this drug and overcome resistance, thereby improving the outcomes of myeloma patients.

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