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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.

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.

Development of Novel Types of Proteasome Inhibitors that Regulate Substrate
Year Awarded: 2008 Type of Grant: Senior Research Awards
Location: United States Institution: Harvard Medical School
Amount: $200,000 Investigator: Alfred Goldberg
Velcade (Bortezomib) is a successful new treatment for Multiple Myeloma. It acts by inhibiting the function of the proteasome--a cellular machine for protein degradarion that plays critical roles in the regulation of cell growth. Velcade and two related drugs now in development directly block the proteasome��_s ability to cleave proteins, though Velcade causes unwanted side effects. Recently we have identified a new molecular target for the development of novel types of drugs that block proteins from ever entering the proteasome,and would thus prevent their degradation. We now hope to find small molecules that inhibit this entry step and that may offer advantages over Velcade in cancer therapy.

Targeting a third NF-KB pathway for anti-myeloma drug development.
Year Awarded: 2008 Type of Grant: Senior Research Awards
Location: United States Institution: University of Wisconsin-Madison
Amount: $200,000 Investigator: Shigeki Miyamoto
Multiple myeloma (MM) is a treatable but incurable disease. Although major progress continues to be made in the treatment of MM with the development of new drugs, such as bortezomib and lenalidomide, drug resistance is still the major hurdle that inevitably results in patient demise. We identified an atypical activation pathway for NF-��_��_B, a family of gene regulators implicated in drug resistance in MM. Our analysis of primary MM samples indicated that this pathway is critically involved. We propose to determine its role in MM and isolate an inhibitor for it to combat this major clinical problem.

Erastin analogs as anti-myeloma agents
Year Awarded: 2008 Type of Grant: Senior Research Awards
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $200,000 Investigator: Constantine Mitsiades
Ras mutations are frequent in advanced myeloma (MM) with resistance to resistance to currently available therapies. Erastin is a compound that selectively kills cells that harbor such mutations and our preclinical work with PRLX93936, a compound derived from erastin, shows its potent activity against MM cells both in laboratory cultures and animal studies. In this project, we will identify molecular markers that can help predict which MM patients will respond to PRLX93936 and develop potent and safe combinations of this agent with other anti-MM drugs, with the ultimate goal to help the design of future clinical trials of PRLX93936, or other agents of this class of drugs, for MM treatment.

Overcoming drug resistance in MM: development of an in vivo mouse model
Year Awarded: 2008 Type of Grant: Senior Research Awards
Location: International Institution: University of Wuerzburg
Amount: $200,000 Investigator: Ralf Bargou
Multiple myeloma (MM) still is an uncurable cancer of the haematological system. The vast majority of patients will relapse after initial treatment and finally succumb to their disease. Thus, the development of drug resistance during the course of the disease is the major clinical problem to be solved in MM. Recently, we have identified an oncogene, designated YB-1, that is assumed to play a key role in the development of drug resistance. Therefore, we will now analyze the role of YB-1 establish in an MM animal in order to develop targeted therapeutic strategies to overcome drug resistance in MM.

Investigation of TP53-regulated microRNAs and mRNAs in multiple myeloma
Year Awarded: 2008 Type of Grant: Research Fellow Awards
Location: United States Institution: University of Arkansas
Amount: $75,000 Investigator: Wei Xiong
Resistance to programmed cell death (apoptosis resistance) is a significant contributing factor to cancer therapy failure. One way to overcome this phenomenon is through modulation of genes that influence apoptosis. We will examine the TP53 gene and its influence on other gene targets, such as small molecules called microRNAs in multiple myeloma (MM). Loss of TP53 expression correlates with poor outcome in MM. We have identified 25 microRNAs in MM that are altered by TP53 expression. Investigation of these small molecules will provide an insight into their role in myeloma progression, use in prognostics, and potential therapeutic targets.

Phosphoproteomic analysis of NF-kappaB in MM
Year Awarded: 2008 Type of Grant: Senior Research Awards
Location: United States Institution: Michigan State University
Amount: $200,000 Investigator: Jetze Tepe
This project aims at better understanding the reaction of multiple myeloma cells to specific chemotherapies. Addition of phosphate groups at specific positions on the protein p65 induces synthesis of other proteins that control cell survival, and this work will identify changes in the number and position of phosphate groups on p65 as a function of disease stage, chemotherapeutic treatment, and treatment resistance. This knowledge may allow rational combination of several chemotherapeutic treatments. These studies will include investigations of a recently developed compound that shows both low toxicity in healthy cells and extremely high efficacy in combination therapies.

Vaccination and T cell therapy Using DC/Myeloma fusions with Transplant
Year Awarded: 2008 Type of Grant: Senior Research Awards
Location: United States Institution: Beth Israel Deaconess Medical Center
Amount: $200,000 Investigator: David Avigan
We developed a patient specific cancer vaccine comprised of immune stimulating cells fused with patient derived myeloma cells. We have shown that vaccination with fusion cells stimulates the immune system to target and eliminate myeloma cells. We will examine whether vaccination prior to and following stem cell transplantation more effectively stimulates anti-tumor immune responses and eliminates the small number of chemotherapy resistant myeloma cells that commonly survive after transplant. We will collect immune cells from patients who been vaccinated and examine a strategy to expand anti-tumor cells in the laboratory to further enhance the effectiveness of the vaccine.

Define CKS1B signaling pathways in myeloma: Therapeutic implication
Year Awarded: 2008 Type of Grant: Senior Research Awards
Location: United States Institution: University of Arkansas
Amount: $200,000 Investigator: Fenghuang Zhan
Multiple myeloma still remains incurable. Specific genetic abnormalities in myeloma cells were believed to play an important role in myeloma progression. We recently found that high-expression of CKS1B in myeloma cells is such a genetic abnormality which could be linked to early disease-related death. Interestingly, CKS1B gene ablation will kill myeloma cells and inhibit tumor growth in myeloma-bearing mice. This indicates that CKS1B and the downstream signaling pathways responsible for the induction of myeloma cell death are potential therapeutic targets for high-risk myeloma disease. We now propose to identify and characterize these CKS1B-mediated downstream signaling pathways.

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