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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.

Chromatin Writers, Readers and Erasers in Multiple Myeloma
Year Awarded: 2013 Type of Grant: Epigenetics Program Project Grant
Location: United States Institution: Northwestern University - Chicago Campus
Amount: $1,500,000 Investigator: Jonathan Licht
Multiple myeloma can be caused by abnormal gene regulation, leading to uncontrolled cell growth. This can result from mutation of regulatory proteins that chemically modify genes to control their expression. There are specific proteins that “write” these chemical changes, others that bind to the modified genes, “reading” the chemical signal to turn the gene on or off, while a third set of proteins can “erase” the chemical modification. This multi-institutional and international program project grant being led by Dr. Jonathan D. Licht at the Robert H. Lurie Comprehensive Cancer Center, Northwestern University, and scientists and clinicians from the Dana Farber Cancer Institute in Boston, the Peter MacCallum Cancer Centre in Melbourne Australia and the San Raffaele Scientific Institute in Milano Italy will study all three classes of proteins at the molecular level, verify that the abnormal proteins cause MM and discover therapies to treat MM by reversing abnormal gene regulation.

TJP1: A Novel Modulator of Proteasome Inhibitor Sensitivity and Resistance
Year Awarded: 2013 Type of Grant: Research Fellow Awards
Location: United States Institution: University of Texas M.D. Anderson Cancer Center
Amount: $75,000 Investigator: Xingding Zhang
Proteasome inhibitors play a central role in myeloma therapy, but we have no way to identify patients with sensitive or resistant disease. My studies have identified the novel gene TJP1 as a modulator of proteasome inhibitor sensitivity and resistance. Additional studies are planned to better understand how TJP1 exerts these effects, and to determine if TJP1 is a biomarker that predicts which patients will respond to bortezomib- or carfilzomib-based therapy. Finally, new approaches targeting TJP1 which may enhance activity and overcome resistance to proteasome inhibitors will be evaluated pre-clinically to provide a basis for their future use in the clinic. We thank Amgen, Celgene, Genentech, Millennium and Onyx for their generous support of this award.

Reversing Malignant Reprogramming of Multiple Myeloma Cancer Stem Cells
Year Awarded: 2013 Type of Grant: Research Fellow Awards
Location: United States Institution: University of California, San Diego
Amount: $75,000 Investigator: Leslie Robertson
Multiple myeloma is the second most common blood cancer, with over 20,000 new cases diagnosed annually. Despite intensive treatments, multiple myeloma remains incurable as a result of drug-resistant dormant cancer stem cells that reside in the malignant bone marrow. Disease progression is highly dependent on inflammatory cues from the microenvironment. The overall goals of this project are to investigate the role of the inflammation-responsive stem cell pathways Notch and ADAR1 in multiple myeloma cancer stem cell reprogramming, and to develop more effective therapeutic strategies that selectively target malignant stem cells in primary patient samples and pre-clinical models. We thank Amgen, Celgene, Genentech, Millennium and Onyx for their generous support of this award.

The role of hypoxia in the micro-residual disease in multiple myeloma
Year Awarded: 2013 Type of Grant: Research Fellow Awards
Location: United States Institution: Washington University in St. Louis
Amount: $75,000 Investigator: Barbara Muz
Micro-residual disease is a cell population which remains after therapy. These cells change their properties to become stem-cell-like and, therefore, become more difficult to treat. These cells have the capability of self-renewal to restart the disease and cause the relapse. This population was not well identified and characterized in multiple myeloma. We propose the presence of this population in myeloma, and we hypothesize that the reason for its development is the lack of oxygen in rapidly growing tumors (tumor-hypoxia). We further propose to inhibit tumor-hypoxia as a therapeutic target to increase sensitivity to therapy and prevent relapse of multiple myeloma. We thank Amgen, Celgene, Genentech, Millennium and Onyx for their generous support of this award.

Novel regulatory properties of proteasomes in multiple myeloma
Year Awarded: 2013 Type of Grant: Research Fellow Awards
Location: United States Institution: Harvard Medical School
Amount: $75,000 Investigator: Nikolay Kukushkin
Drugs blocking proteasome function are especially toxic to multiple myeloma cells and have greatly advanced the treatment of this disease. Nevertheless, the specific properties of proteasomes in myeloma cells have never been rigorously analyzed, although they may contribute to the special sensitivity of these cells to proteasome inhibitors. We recently discovered that proteasome inhibition triggers a chemical modification of these particles that further inactivates them. This inactivation mechanism must contribute to the efficacy of proteasome inhibitors. I hope to define its biochemical mechanism and the specific properties of proteasomes from myeloma cells, which hopefully will provide basis for development of improved treatments. We thank Amgen, Celgene, Genentech, Millennium and Onyx for their generous support of this award.

Pre-clinical Study of Daratumumab in auto-SCT for MM and AL amyloidosis
Year Awarded: 2013 Type of Grant: Research Fellow Awards
Location: United States Institution: Tufts Medical Center
Amount: $75,000 Investigator: Chakra Chaulagain
Monoclonal antibodies can act with a patient’s immune cells to kill cancer but there is no monoclonal for myeloma. Daratumumab, a monoclonal now being tested for myeloma, recently received “Breakthrough” designation from the FDA because of activity in an early clinical trial. Daratumumab binds myeloma cells causing their death by acting with patient immune cells. We are studying daratumumab and stem cell transplantation using immune cells from myeloma patients undergoing transplant. Using daratumumab in stem cell transplantation may eliminate residual myeloma cells and prolong survival. Our study will provide a basis for testing this combination in a clinical trial. We thank Amgen, Celgene, Genentech, Millennium and Onyx for their generous support of this award.

Immunotherapy after ASCT for MM using MAGE-A3/Poly-ICLC-primed T-cells
Year Awarded: 2013 Type of Grant: Senior Research Awards
Location: United States Institution: The University of Maryland
Amount: $200,000 Investigator: Aaron Rapoport
Our long-term goal is to develop a highly effective method for helping the patient’s immune system to recognize and attack myeloma cells in order to increase the chance for remission and even cure. We have previously found that giving back patient immune “T-cells” which were expanded in the laboratory leads to better immune system recovery after high-dose chemotherapy. In this new study, we are testing whether this approach can be further improved by using a possible new myeloma vaccine for a protein/marker called “MAGE-A3” in combination with two new agents that “turn-on” the immune system – Poly-ICLC and lenolidomide. We thank the Holway family for their generous support of this award.

Treating multiple myeloma using anti-CD138 genetically fused to type 1 IFN
Year Awarded: 2013 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 (IFNs) are proteins that can inhibit the growth of and kill cancer cells. Antibodies are available that recognize the CD138 protein present on the surface of all multiple myeloma (MM) cells. We will now join IFN to these MM-specific antibodies thereby creating a “magic bullet” that will specifically target IFN to the site of the tumor where it will cause the tumor to die. We will be also determine if there is even more cancer cell death when this “magic bullet is used in combination with bortezomib or lenalidomide, drugs FDA approved for the treatment of MM. We thank the Assink family for their generous support of this award.

The Role of MDSCs in the Immune Escape of Multiple Myeloma
Year Awarded: 2012 Type of Grant: Research Fellow Awards
Location: United States Institution: H. Lee Moffitt Cancer Center and Research Institute
Amount: $75,000 Investigator: indu ramachandran
In Multiple myeloma (MM), as tumor expands in the bone marrow (BM), the ability of immune effector cells to kill tumor cells is inhibited through unclear mechanisms. In experimental MM models, we see the development of myeloid-derived suppressor cells (MDSCs), an inhibitory cell type that negatively regulates immune effector cell function. A reduction in MDSC levels resulted in improved survival of mice with MM. Thus, we will test the hypothesis that MDSCs promote MM growth by inhibiting BM immunological responses against MM. This study could provide validation for the therapeutic-targeting of MDSCs in order to improve anti-MM immunity in patients.

Understanding the resistant plasma cell: the dream of curing Myeloma
Year Awarded: 2012 Type of Grant: Research Fellow Awards
Location: International Institution: Instituto de Biologia Molecular y Celular del Cancer (CSIC-USAL)
Amount: $75,000 Investigator: Bruno Paiva
Multiple myeloma is the second most frequent hematological malignancy and yet incurable, as all patients eventually become resistant to treatment. This is partly explained by the presence of tumor cells that persist after therapy, and that are usually detectable using highly sensitive techniques. Our group has a leadership position in the detection of persistent myeloma cells after treatment; now, we want to go a step further and fully characterize these cells. It is our belief that a first-ever characterization of myeloma chemoresistant cells will contribute to identifying the hidden clues to overcome chemoresistance, and finally achieve a cure in this disease.

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