The Vera and Joseph Dresner Foundation is pleased to announce its third annual Myelodysplastic Syndrome (MDS) Research Fund grant recipients. Grants were awarded to The Cleveland Clinic Foundation, Memorial Sloan-Kettering Cancer Center, and the University of Miami. These grants totaling $1,000,000 support the research of two early career investigators and one established career investigator. The principle goal of the research fund is to support cutting-edge MDS research and related programs that will lead to the future standards of care and ultimately, a cure.
“These grants from the Vera and Joseph Dresner Foundation will advance exciting research into the biology of MDS as well as optimize treatment strategies, particularly within older adults. Our goal continues to be eliminating these diseases and improving the lives of MDS patients,” said Dr. Mikkael A. Sekeres of Cleveland Clinic and Chair, MDS Research Fund Scientific Advisory Board. Virginia Romano, the Foundation’s Chief Executive Officer said, “The Foundation is pleased to continue to support nationwide institutions that seek to develop improved MDS treatment modalities.”
Memorial Sloan-Kettering Cancer Center received a grant to support the early career work of Dr. Richard J. Lin. Dr. Lin will be working closely with his mentor, Dr. Sergio A. Giralt. The goal of the research is to evaluate the efficacy of an adopted strategy based on geriatric vulnerabilities and geriatric management to reduce non-relapse mortality for older MDS patients receiving curative intent allogeneic hematopoietic transplantation.
The second early career grant was awarded to Dr. Luisa Cimmino, through the University of Miami. Dr. Cimmino, working closely with her mentor Dr. Stephen Nimer, will assess the role of vitamin C in the maintenance of TET enzymatic activity during MDS progression and treatment.
The Cleveland Clinic Foundation was awarded a grant to support
Dr. Richard A. Padgett, an established investigator. This research will attempt to show the use of the characterization of DDX41 perturbed cells and animals provide rational targets for therapeutic approaches to treat splicing factor mutated MDS.