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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.

Quantification of Circulating Tumor Specific DNA in Multiple Myeloma
Year Awarded: 2010 Type of Grant: Diagnostic Investment Awards
Location: United States Institution: Johns Hopkins University
Amount: $500,000 Investigator: William Matsui

Identification of molecular targets in myeloma microenvironments
Year Awarded: 2010 Type of Grant: Tumor Microenvironment
Location: United States Institution: University of Arkansas
Amount: $249,987 Investigator: Ya-Wei Qiang
Myeloma can control its bone marrow (BM) microenvironment, ensuring its survival and making it extremely difficult to treat. Our previous studies have demonstrated that cadherins abnormally occur in myeloma and BM stromal cells. We believe that cadherins promote myeloma growth, survival and drug resistance by enhancing their interaction with the BM microenvironment. We will study the role of cadherins in such process and then study strategies to interfere with their signaling. These studies will not only benefit understanding the role of cadherins in the biology of myeloma, but more importantly will help design new therapeutic strategy.

Understanding the Myeloid Microenvironment in Multiple Myeloma
Year Awarded: 2010 Type of Grant: Tumor Microenvironment
Location: United States Institution: Health Research Incorporated, Roswell Park Cancer Institute Division
Amount: $250,000 Investigator: Kelvin Lee
Multiple myeloma cells have to interact with normal bone marrow cells to survive, and these interaction may be new targets for treatment. We have found that the CD28 molecule on myeloma cells helps them survive by binding to its partner molecules CD80 and CD86 on bone marrow myeloid immune cells - eliciting factors that support myeloma growth and survival, conferring chemotherapy resistance and suppressing the immune system. Targeting the myeloid cells and molecules involved may reverse this effects, and we proposed to test this strategy in animal models of myeloma to develop a new treatment strategy for multiple myeloma.

Consequences of KDM6A/UTX loss in multiple myeloma
Year Awarded: 2010 Type of Grant: Target Credentialing
Location: United States Institution: The Translational Genomics Research Institute
Amount: $250,000 Investigator: Jonathan Keats
A gene called UTX is frequently lost in multiple myeloma, however, we do not know the significance of this event. This gene is required to remove a specific chemical alteration from the scaffold that winds and packs our DNA into the nucleus of each cell. This chemical modification prevents a gene from being expressed. Our hypothesis is that a number of genes, which should be turned on to prevent the development of the tumor, are stuck in the off position because UTX is not functioning properly. The goal is to identify these genes and potential downstream therapeutic targets.

Elucidation of Therapeutic Targets in MMSET-associated Myeloma
Year Awarded: 2010 Type of Grant: Target Credentialing
Location: United States Institution: Northwestern University - Chicago Campus
Amount: $250,000 Investigator: Jonathan Licht
Multiple Myeloma (MM) is a tumor of antibody-producing white cells accounting for up to 10% of blood cancers. MMSET is a protein abnormally turned on in 15% of MM patients. MMSET can stimulate growth of myeloma cells and turn on and off hundreds of genes. We identified a set of genes turned on in MMSET associated myeloma that may be critical for this tumor grow, invade and survive chemotherapy treatments. We will prove the importance of a number of these genes in order to determine whether the proteins they make could represented new targets for therapy in MM.

Regulation of multiple myeloma by myeloid cells
Year Awarded: 2010 Type of Grant: Tumor Microenvironment
Location: United States Institution: H. Lee Moffitt Cancer Center and Research Institute
Amount: $250,000 Investigator: Yulia Nefedova
Recent studies have demonstrated that tumor growth is accompanied by impaired differentiation of myeloid cells in bone marrow resulting in accumulation of cells known as myeloid-derived suppressor cells (MDSC). These cells have a remarkable ability to suppress immune response against tumor and therefore promote tumor progression. Although role of MDSCs in solid tumors has been studied extensively, their role in hematological malignancies including multiple myeloma (MM) is still unknown. In this proposal, we will investigate the role of MDSCs in MM growth and chemoresistance and test whether targeting of these cells could be beneficial for MM treatment.

The role of XBP1s in multiple myeloma microenvironment
Year Awarded: 2010 Type of Grant: Tumor Microenvironment
Location: United States Institution: University of Pittsburgh
Amount: $249,950 Investigator: Hongjiao Ouyang
Bone marrow stromal cells (BMSCs) play an important role in supporting multiple myeloma (MM) cell growth and facilitating bone resorption in multiple myeloma bone disease. We will study the factors produced and induced by MM cells that increase the capacity of BMSCs to support MM cell growth. In addition, we will study if Resveratrol, a constituent of red wine, could repress the capacity of BMSCs to support MM tumor growth and facilitate bone resorption for treating myeloma.

Development of combination regimens based on histone deacetylase inhibitors
Year Awarded: 2010 Type of Grant: Validation of Novel Compounds and Combinations
Location: United States Institution: Dana-Farber Cancer Institute
Amount: $200,000 Investigator: Constantine Mitsiades
The expression of several cancer genes and the function of their respective proteins is influenced by histone deacetylases (HDAC). Drugs that inhibit these enzymes can kill myeloma cells in the laboratory or render them more vulnerable to other therapeutics. In this project, we will identify anti-cancer agents the activity of which is enhanced by HDAC inhibitors. We will also identify molecular markers that can help predict which MM patients may respond better to these combinations. The ultimate goal will be help the design of future clinical trials of combinations that incorporate HDAC inhibitors for the treatment of MM.

Targeted inhibition of JAK-STAT signalling to modify MM drug resistance
Year Awarded: 2010 Type of Grant: Validation of Novel Compounds and Combinations
Location: International Institution: Monash University
Amount: $197,308 Investigator: Andrew Spencer
This project will study the ability of a new drug CYT387. CYT387 was specifically designed to prevent the activity of a critical protein JAK, to kill myeloma tumour cells. CYT387 has been evaluated in the clinic for safety and efficacy in the treatment of other forms of blood cancer, Myeloproliferative Disorders. The project will specifically determine what other drugs when combined with CYT387 lead to the highest level of killing of both laboratory myeloma cells and those from myeloma patients. Once identified these combinations can then be introduced into new clinical trials of myeloma treatment.

Glycosphingolipid inhibitors in the treatment of multiple myeloma
Year Awarded: 2010 Type of Grant: Validation of Novel Compounds and Combinations
Location: International Institution: Imperial College of Science, Technology and Medicine
Amount: $196,433 Investigator: Anastasios Karadimitris
Multiple myeloma is an incurable cancer of the blood. Destruction of the bone caused by over-activation of the bone cells osteoclasts with consequent severe pain and impaired mobility affects most patients with myeloma. Based on extensive experimental work we found that a medicine called Miglustat can stop activation of osteoclasts. We propose to test whether Miglustat is effective in treating bone disease in mice with myeloma. If this is the case then we can swiftly test Miglustat in patients with myeloma because it is already approved for use in a disease called Gaucher��_s disease

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