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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.

Targeting Vascular Endothelial Growth Factor for Treatment of Myeloma
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: Mayo Clinic Rochester
Amount: $200,000 Investigator: Shaji Kumar
The future of myeloma therapy lies in our ability to rationally combine drugs acting through different mechanisms against myeloma cells. We are in the process of conducting a clinical trial combining Sorafenib (destroys tumor associated blood vessels) and Revlimid (kills tumor cells directly). We propose to use samples from patients enrolled in the trial to study the mechanisms by which these drugs destroy tumor cells, as well as how tumor cells resist the treatment in patients who do not benefit will allow us to improve and develop better treatments and thus the outcome for patients with myeloma.

Genetic screen to identify Wnt target genes to treat Myeloma
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $200,000 Investigator: Ruben Carrasco
Multiple Myeloma (MM) is a cancer involving cells that normally comprise a small population in the bone marrow. In this disease, however, certain changes in the genetic information of the cells causes them to multiply in number and become malignant, ultimately leading to extensive morbidity and mortality. At this time, there is no cure for MM and 90% of patients die within 10 years. We are working to find a cure for this devastating disease. In our previous studies we have found genetic abnormalities that may be responsible for the disease. We have identified one such abnormality in many patients pointing to aberrant cellular processes responsible for tumor growth and the ability of the cancer cells to home and spread within the bone marrow microenvironment. We would like to identify new and more specific drug targets within the Wnt signaling pathway, a cellular signaling pathway we have found to be dysregulated in MM cells. We will validate these drug targets in mice with the intent of developing therapies for future use in patients.

Mechanism and efficacy of cyproheptadine as a novel anti-myeloma agent
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: International Institution: University Health Network
Amount: $200,000 Investigator: Aaron Schimmer
Increased levels of cyclin D2 are associated with chemoresistance in myeloma. Through high throughput screening, we identified the off-patent appetite stimulant cyproheptadine as an inhibitor of the cyclin D2 promoter, respectively. Subsequent studies determined that cyproheptadine killed myeloma cells. Here, we propose to: 1) Determine the mechanism of action of cyproheptadine. 2) Initiate the preclinical development of cyproheptadine as a novel treatment of multiple myeloma. 3) Identify the binding targets for cyproheptadine.

Stem cell rejection to induce anti-tumor immunity
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: Massachusetts General Hospital (The General Hospital Corp.)
Amount: $200,000 Investigator: Megan Sykes
With a reduced toxicity bone marrow transplant developed at our institution, approximately 1/3 of patients rejected their graft. Surprisingly, some of those patients achieved remissions of advanced malignancies. Animal experiments suggest that anti-tumor effects result from tumor-specific immune responses fueled by the rejection of donor marrow. We propose a clinical protocol in which graft rejection will be intentionally induced following a very low toxicity transplant by giving previously collected patient white cells (lymphocytes) after their transplant. Patients with mismatched (haploidentical) family donors and who have no good therapeutic alternatives will be considered. Safety and anti-tumor responses will be evaluated.

The role of SCF ubiquitin ligases in Multiple Myeloma
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: New York University School of Medicine
Amount: $200,000 Investigator: Michele Pagano
Cells ordinarily remove proteins by destroying them. Cells will tag a protein by attaching a ubiquitin molecule, and the proteasome complex searches out and destroys ubiquitin-tagged proteins, like a garbage truck collecting trash. Too much destruction of tumor suppressors can lead to cancer. Recently, three genes for proteins responsible for tagging proteins with ubiquitin (Fbxo3, Fbxo9, and Fbxo32) were found to be overexpressed in Multiple Myeloma (MM), suggesting a role of these proteins in the destruction of tumor suppressors and MM development. This proposal seeks to determine the role of these proteins and their substrates in MM.

Therapeutic targeting of Notch and bcl-2/bcl-xL in multiple myeloma
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: H. Lee Moffitt Cancer Center and Research Institute
Amount: $200,000 Investigator: Yulia Nefedova
Resistance of myeloma cells to chemotherapy still remains one of the serious clinical problems. Activation of Notch signaling in myeloma cells is one of the mechanisms of their drug resistance. Blocking of Notch pathway with specific inhibitor resulted in myeloma cell death and increased myeloma cell sensitivity to chemotherapeutics. Recently developed ABT-737 induces myeloma cell death by targeting bcl-2 and bcl-xL. We hypothesized that combination of these two drugs which have distinct downstream targets responsible for the induction of cell death will have profound anti-myeloma effect and significantly increase sensitivity of myeloma cells to conventional chemotherapeutics.

Refinement of the XBP-1 mouse model of multiple myeloma
Year Awarded: 2007 Type of Grant: Animal Model
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $200,000 Investigator: Yaoqi Wang
The availability of a multiple myeloma (MM) mouse model will afford the MM community with enhanced opportunities in the elucidation of the functional role of specific mutations, the discovery of new MM-relevant genes by genomic technologies, and the availability of a preclinical model for designing and assessing target-based therapeutic approaches. We have recently developed the first transgenic animal model of MM. However, only about 30% of these mice developed MM with long latency. In this grant, we propose to refine this model further to generate a highly susceptible MM model which will have great preclinical utilities in drug development.

A transgenic model of multiple myeloma
Year Awarded: 2007 Type of Grant: Animal Model
Location: United States Institution: University of Pittsburgh
Amount: $200,000 Investigator: PREET CHAUDHARY
The Nuclear Factor kappaB (NF-kB) pathway is active in myeloma cells. In order to examine whether this pathway plays a role in myeloma development and in determining the response to treatment, we will develop transgenic mice in which the NF-kB pathway is activated in the plasma cells. We will study whether these mice develop disease similar to myeloma and whether presence of activated NF-kB influences their response to commonly used antimyeloma drugs, such as Melphalan and Bortezomib. These studies will not only lead to a better understanding of myeloma development but also provide novel predictive markers of response to therapy.

Novel Combination Therapies for Mutiple Myeloma
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: The University of Alabama at Birmingham
Amount: $200,000 Investigator: Yang Yang
General Audience Abstract: Briefly describe your proposed project in 100 words or less. Be sure to use language that can be easily understood by a general audience. Current anti-myeloma drugs can not kill all tumor cells. Heparanase is an enzyme that rarely exists in normal tissue but is preferentially expressed in human tumors including multiple myeloma (MM). Our previous experiments demonstrated that heparanase promotes growth and metastasis of MM ; and a heparanase inhibitor, 100NA,RO-H dramatically suppresses myeloma tumor growth in animal models of MM . Because 100NA,RO-H targets different mechanism of tumor growth, compare to current anti-myeloma drugs, we will investigate, in present study, if adding 100NA,RO-H to clinic anti-myeloma drugs can more effectively kill tumor cells and improve MM patients��_ survival in the future.

Cell cycle based combination therapy for multiple myeloma
Year Awarded: 2007 Type of Grant: Senior Research Awards
Location: United States Institution: Joan and Sanford I. Weill Medical College of Cornell University
Amount: $200,000 Investigator: Selina Chen-Kiang
Myeloma is treatable but incurable because current therapies can��_t successfully control cancer cell division. We have identified two novel therapeutic targets that promote cancer cell division, Cdk4 and Cdk6, and demonstrated that they are completely inhibited in patient myeloma cells by PD 0332991, an orally bioactive small molecule. PD 0332991 also prevents human myeloma tumor growth in animal models, and strikingly enhances the killing of myeloma cells by other therapies. A randomized Phase I/II clinical trial for PD 03332991-Velcade will soon be initiated. This work will complement the trial and advance the development of PD 0332991-based combination therapy.

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