/content/dam/www/people-profile-photos/d/joachim-deeg/joachim-deeg-d.jpg
Deeg
H. Joachim Deeg, MD
- Professor Emeritus, Clinical Research Division, Fred Hutch
- Professor Emeritus, University of Washington
Background
Dr. Joachim Deeg is an expert in bone marrow failure and blood and bone marrow cancers. He is interested in how leukemia develops, especially via a precancerous blood disorder called myelodysplastic syndrome, or MDS. His research encompasses pathophysiology, genetics and gene regulation of this disorder and its progression to leukemia. He also leads clinical trials of new treatment approaches for MDS. He has established bone marrow transplantation from healthy donors as a curative therapy for MDS, aplastic anemia and a group of blood cancers called myeloproliferative neoplasms. Dr. Deeg has also worked extensively in animal models and developed a regimen, adopted worldwide, for the prevention of graft-vs.-host disease, or GVHD, a common and potentially dangerous complication of blood stem cell transplantation. His recent studies have included the use of alpha-1 anti-trypsin to treat GVHD. Dr. Deeg is also interested in the ethics of decision-making regarding the optimal treatment strategy for a given patient.
Visiting Professor
Carl Carus University, Dresden, Germany
Clinical Expertise
Diagnosis and treatment (transplant, non-transplant) of Aplastic anemia, Myelodysplastic syndromes, Myeloproliferative neoplasms. Prevention and treatment of GVHD.
Education
Wilhelms Universitaet, Bonn, Germany, Dr.med. (MD), 1972
Research Interests
Pathophysiology, genetics and epigenetics of MDS and myeloproliferative disorders.
Inflammatory responses and GVHD (effects of alpha1 anti-trypsin [AAT])
How to deal with uncertainty when counseling patients.
Current Projects
Novel molecular risk factors in patients with chronic myelomonocytic leukemia (CMML) and myeloproliferative neoplasms.
Novel treatment strategies for patients with MDS.
Alpha 1 anti-trypsin for treatment and prophylaxis of GVHD.
Transplantation for myeloproliferative neoplasms in the age of JAK2 inhibitors.