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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.

Combination of PARP and Proteasome Inhibitors in Multiple Myeloma
Year Awarded: 2011 Type of Grant: Senior Research Awards
Location: International Institution: University of Calgary
Amount: $200,000 Investigator: Nizar Bahlis

Overcoming Lenalidomide Resistance in Multiple Myeloma
Year Awarded: 2011 Type of Grant: Research Fellow Awards
Location: United States Institution: The Univeristy of Texas-MD Anderson Cancer Center
Amount: $75,000 Investigator: Chad Bjorkland
Multiple myeloma (MM) is an incurable type of blood cancer that will be diagnosed in more than 20,000 individuals in the U.S. this year alone. Novel cancer drugs like lenalidomide (Revlimid��_) have greatly increased the survival rate and quality of life for those afflicted with myeloma. Unfortunately, most patients will eventually relapse and the disease will progress. Our lab has identified a cell signaling pathway that is at least partially responsible for lenalidomide-associated drug resistance in MM. This proposal aims to evaluate the potential clinical effectiveness of targeting this pathway to reduce or reverse lenalidomide drug resistance in MM.

Targeting DEPTOR in multiple myeloma
Year Awarded: 2011 Type of Grant: Research Fellow Awards
Location: United States Institution: Brentwood Biomedical Research Institute
Amount: $75,000 Investigator: yonghui yang
The DEPTOR protein is singularly present only in multiple myeloma cancer cells (no other malignancies). It affects many signal pathways that support viability and proliferation of the tumor cells. Genetically deleting DEPTOR kills myeloma cells. Thus, we plan to develop new drugs that inhibit DEPTOR function with the goal of inducing death of myeloma cells.

Determining the role of the histone demethylase gene JMJD1C in myeloma
Year Awarded: 2011 Type of Grant: Research Fellow Awards
Location: United States Institution: The Translational Genomics Research Institute
Amount: $75,000 Investigator: Bodour Salhia
Increasing evidence from our lab and others is pointing toward the importance of epigenetic deregulation in multiple myeloma (MM). Epigenetic modifications involve changes to DNA that are independent of the sequence. We recently analyzed gene expression data and identified the epigenetic gene JMJD1C to be differentially expressed in a large percentage of MM. To date its role in myeloma development is unknown. The current proposal aims to determine the molecular and biological significance of JMJD1C in MM and to test the overarching hypothesis that inhibition of JMJD1C is deleterious to MM cell growth.

Small molecule inhibitors of STAT3 in Multiple Myeloma
Year Awarded: 2011 Type of Grant: Research Fellow Awards
Location: International Institution: Princess Margaret Hospital
Amount: $75,000 Investigator: Victor Jimenez-Zepeda
The Signal Transducer and Activator of Transcription 3 (STAT3) signaling pathway has been implicated in the proliferation, chemoresistance, and survival of multiple myeloma (MM) cells. Despite the advent of novel agents including lenalidomide and bortezomib, however, the disease remains incurable and new therapies are desperately needed. Given the biologic rationale and the preliminary data to date it is not unreasonable to propose that effective anti-MM therapy can come from inhibiting persistently active Stat3. The aim of this proposal is to validate the first ��_drug-like��_ Stat3 inhibitors of therapeutic utility against MM and to promote their progression to clinical trial.

Validation of Potential Driver Mutations in Multiple Myeloma Cohort
Year Awarded: 2011 Type of Grant: Research Fellow Awards
Location: United States Institution: Mayo Clinic Arizona
Amount: $75,000 Investigator: Jan Egan
Patients treated for multiple myeloma can become unable to respond to the drugs used to treat their cancer. Our goal is to study changes in the genetic material of the cancer and how that may be causing the cancer to no longer respond to the drug treatment. First, we will look for changes in the genome in a small group of patients who no longer respond to their drug treatment. Once these changes are found, we will see how common they are and if they may be preventing the drugs from working.

Improved Therapeutics: Targeting Sdc1/Integrin Pathways with SSTN
Year Awarded: 2011 Type of Grant: Research Fellow Awards
Location: United States Institution: University of Wisconsin-Madison
Amount: $75,000 Investigator: Valerie Trapp
I study three important proteins that form a signaling complex vital for myeloma cell invasion and survival. A newly described inhibitory peptide, called synstatin, blocks formation of this complex. I find that regulation of the complex in myeloma cells also requires activation of a fourth protein, �_�4�_�1 integrin, known to play important roles in myeloma disease progression and resistance to chemotherapy. I will test whether synstatin disrupts two tumor-promoting mechanisms known to rely on �_�4�_�1 integrin activation: the extravasation of myeloma cells across endothelial cell monolayers and cell adhesion-mediated drug resistance.

Is N-cadherin expression a prognostic indicator in multiple myeloma?
Year Awarded: 2011 Type of Grant: Research Fellow Awards
Location: United States Institution: Institute of Medical and Veterinary Science
Amount: $75,000 Investigator: Kate Vandyke
We have found that the cell adhesion protein N-cadherin is present at high concentrations in the blood of myeloma patients with aggressive disease and a poor response to therapy. This proposal will determine whether measuring plasma N-cadherin levels is a viable prognostic test to identify these patients. We will use in vitro experiments and a mouse model of myeloma that mimics human disease to determine the role played by N-cadherin in disease development. Finally, we will conduct preclinical testing of the therapeutic efficacy of a drug that inhibits N-cadherin function in controlling disease progression in high-risk myeloma patients.

Cereblon control of IMiD function
Year Awarded: 2011 Type of Grant: Senior Research Awards
Location: United States Institution: Mayo Clinic Arizona
Amount: $200,000 Investigator: Alexander Stewart
The anti-myeloma drugs Thalidomide, Lenalidomide and Pomalidomide are profoundly active in the treatment of Multiple Myeloma and related diseases. Nevertheless, only 30-40% of relapsed patients respond to therapy and most will eventually become resistant. A landmark paper has recently described that the target of thalidomide in cells, responsible for birth defects is called, cereblon (CRBN). We have, conclusively demonstrated that absence of CRBN is also responsible for the action of the IMiDs in Myeloma. The hypothesis is that monitoring CRBN levels will equate with IMiD response and that downstream effects of CRBN function inhibition must explain the activity of these drugs in Myeloma patients.

The Role of MMSET in Regulation of Chromatin Structure in t(4;14)+ Myeloma
Year Awarded: 2011 Type of Grant: Research Fellow Awards
Location: United States Institution: Northwestern University - Chicago Campus
Amount: $75,000 Investigator: Relja Popovic
Despite the discovery of several new therapies, multiple myeloma is an incurable disease. Recently, chromosomal abnormalities, causing the shuffling of genes, were noted to be a root cause of many cases of myeloma. One such abnormality causes the expression of protein called MMSET to be greatly increased. High levels of MMSET induce further chromosomal changes leading to misregulation of pathways important in myeloma development. Our study will identify the genes that are affected by MMSET action and the mechanism by which MMSET induces chromosomal alterations. This could lead to development of strategies that prevent the cancer causing action of MMSET.

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