The International Myeloma Foundation (IMF) will present its 2019 Research Grant awards at a ceremony to be held during the 59th annual meeting of the American Society of Hematology (ASH) in December 2018 at San Diego, California, USA.
Senior Grant Recipients
Djordje Atanackovic, MD
Huntsman Cancer Institute
​Salt Lake City, UT
Anti-CD229 Chimeric Antigen Receptor T Cells for the Treatment of Multiple Myeloma

Multiple myeloma (MM) is an incurable blood cancer. It has recently been shown that the immune system is able to control tumor growth and in some cases to even cure cancer. Specifically, immune cells engineered to express chimeric antigen receptors (CAR) that specifically recognize structures on the surface of tumor cells have shown remarkable clinical results in patients with blood cancers. We have discovered a protein specifically expressed on MM cells and developed several CARs recognizing this antigen that are able to kill MM cells. We propose to determine the therapeutic potential of these CARs in vitro and in vivo.

Felipe Prosper, MD
Foundation for Applied Medical Research (FIMA)
Pamplona, Navarra, Spain
Deciphering the role of eRNAs in the pathogenesis of multiple myeloma

Long non-coding RNAs, which include eRNAs, constitute a novel and unexplored mechanism that can regulate the expression of genes, and therefore regulate the fate of a cell. Our previous work suggested that the expression of such elements is altered in MM. In this project, we will identify the set of eRNAS that are altered in MM, and will ascertain how they work to contribute to the malignant phenotype of the MM cell. Identification of eRNAs that are highly expressed in this disease and confer oncogenic properties may represent new therapeutic targets for MM treatment. 

Karin Vanderkerken, PhD
Vrije Universiteit Brussel
Brussels, Belgium
Targeting residual, dormant cancer cells in myeloma: a new approach

Multiple Myeloma (MM) is a blood cancer that remains most often incurable. MM patients relapse due to the presence of residual cancer cells in the bone marrow. Recently, it has been shown that myeloma cells enter a ‘quiescent or dormant’ state and become resistant to chemotherapy that targets proliferating cells. Axl and CS1 are two genes that were identified to be highly upregulated in dormant cells compared to dividing cells. Our objective is to specifically target the residual cancer cells by the development of radiolabeled nanobodies directed against CS1 and Axl.

Junior Grant Recipients
Neelam Bhardwaj, PhD
Huntsman Cancer Institute
Salt Lake City, UT
Generation and validation of a monoclonal antibody against VISTA for the immunomodulatory therapy of multiple myeloma

Multiple Myeloma (MM) is a blood cancer, which in most cases still remains incurable. The immune system can play an important role in controlling tumor growth and even lead to cures. In particular, the use of checkpoint inhibitors has shown remarkable clinical results for patients with solid tumors by improving the anti-tumor response of the patients’ own T cells. We propose to develop a novel checkpoint inhibitor antibody targeting VISTA, an immunosuppressive protein overexpressed in patients with MM. We will use state-of-the-art technology to develop this antibody and validate its therapeutic potential for the treatment of MM.

Arnold Bolomsky, DI (FH)
Dr. Wilhelminen Cancer Research Institute
Vienna, Austria
Targeting of BMI-1 as novel treatment option in multiple myeloma: Examination of PTC-028 as putative anti-myeloma drug in vitro and in vivo

In spite of ongoing progress novel treatment options for multiple myeloma (MM) are urgently needed. In this context, we recently described the tumour promoting gene BMI-1 as attractive drug target in myeloma. Based on these results this study aims to (1) reveal the role of BMI-1 for the growth and survival of MM cells, (2) identify novel BMI-1 partner molecules, (3) clarify the role of BMI-1 in drug resistance and (4) examine the impact of BMI-1 blockade in a MM mouse model. The results of this study intend to lay the groundwork for clinical testing of BMI-1 inhibitors in myeloma.

Jesus Delgado-Calle, PhD
Indiana University School of Medicine
Indianapolis, IN
Bone/bone marrow-targeted inhibition of Notch signaling in combination with glucocorticoid therapy as a novel approach to treat multiple myeloma

Multiple Myeloma (MM) is a blood cancer in which abnormal plasma cells accumulate in the bone marrow, and induce bone destructive lesions that do not repair, cause excruciating bone pain and a high risk of fracture. In this application we will examine whether blocking Notch activation, a specific type of cell communication pathway in MM cells, combined with steroid treatment decreases MM growth and improves the bone disease and muscle weakness caused by MM. Successful completion of these studies could result in the development of new treatments for MM and prevent bone fractures.

Geoffrey M. Matthews, PhD
Dana-Farber Cancer Institute
Boston, MA
Treating myeloma through inducing degradation of BET bromodomain proteins

Multiple myeloma (MM) is an incurable cancer with a clear unmet need for novel therapeutic approaches. Our data suggests that new agents, known as dBET, have strong anti-tumor effects in MM and act by not only reducing the activity of their target protein, but also causing its complete degradation within the tumor cell. This double-pronged approach leads to far greater levels of cancer cell death than traditional inhibitors, including JQ1. Here we aim to better understand how dBET causes the death of MM cells and whether these new agents can override resistance of MM cells to other agents.

Alessandra Romano
Ospedale San Raffaele
Milano, Italy
Exploiting IDO1-GCN2-p62 axis in MM microenvironment to trigger myeloid derived suppressors cells in multiple myeloma

Multiple myeloma is due to uncontrolled proliferation of malignant plasma cells which survive in the bone marrow for a long time. The bone marrow contains a myriad of cell types that could foster the growth and survival of the plasma cells, hampering the immune system thus to hide tumor to immune surveilling cells. We propose to characterize the molecular signaling in immune surveilling cells which deplete essential aminoacids in the bone marrow microenvironment cells as novel therapeutic target, to restore the immune paresis through aminoacid supplementation.

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