afriedman's picture

Main Profile

Full Name and Degrees: 
Alan D. Friedman, M.D.
Member Role: 
Principal Investigator
Institutional affiliation: 
Johns Hopkins University

Dr. Alan Friedman joins the Consortium from Johns Hopkins University where he is Professor of Oncology and Pediatrics. He received his M.D. from Harvard University and did his pediatric internship and residence at Boston Children’s Hospital.  He then came to Johns Hopkins to complete a Fellowship in pediatric hematology/oncology.  During that time he conducted post-doctoral research with Steven McKnight at the Carnegie Institute Department of Embryology before joining the Johns Hopkins Oncology Department faculty in 1989.  He continues to care for pediatric oncology and transplant patients while devoting the majority of his time to research.

Hub Site: 
03-Alan Friedman

Dr. Alan Friedman (Johns Hopkins University) and Dr. John Cooke (Stanford University) will focus on the safe reprogramming and differentiation of adult cells to blood-forming cell lines for eventual application to blood or vascular disorders.

research focus: 

Dr. Friedman’s work focuses on mechanisms through which normal proteins control the formation of bone marrow stem cells and how these stem cells then develop into neutrophils and monocytes.

He is also studying how normal bone marrow cells become transformed into acute myeloid leukemia (AML). The focus is on three transcription factors:

  • RUNX1
  • C/EBPa
  • NF-kB

Dr. Friedman is attempting to build on his basic research to develop useful clinical applications. In particular, in the context of the Consortium he is pursuing means to utilize RUNX1 and cooperating proteins to favor formation of adult HSC or neutrophils from hESC/iPSC for clinical application.  In other work, he is seeking small molecules that interfere with the action of RUNX1 oncoproteins or interaction between C/EBP and NF-kB proteins as potential novel therapies for AML and other malignancies.

Recent publications: 
Paz-Priel I, Houng S, Dooher J, Friedman AD. (2011). C/EBPα and C/EBPα oncoproteins regulate nfkb1 and displace histone deacetylases from NF- κB p50 homodimers to induce expression of NF-κB target genes. Blood; in press. Guo H, Friedman AD. (2011). Phosphorylation of RUNX1 by cyclin-dependent kinase reduces direct interaction with HDAC1 and HDAC3. J. Biol. Chem.; 286:208-215. Jack G.D, Zhang L., Friedman A.D. (2009). M-CSF elevates c-Fos and phospho-C/EBPa(S21) via ERK whereas G-CSF stimulates SHP2 phosphorylation in marrow progenitors to contribute to myeloid lineage specification. Blood 114:2172-80. Wang D., Paz-Priel I., and Friedman A.D. (2009). NF-kB p50 regulates C/EBPa expression and inflammatory cytokine-induced neutrophil production. J. Immunol. 2009; 182:5757-62. Paz-Priel I., Ghosal A.K, Kowalski J., and Friedman A.D. (2009). C/EBPa or C/EBPa oncoproteins regulate the intrinsic and extrinsic apoptotic pathways by direct interaction with NF-kB p50 bound to the bcl-2 and FLIP gene promoters. Leukemia 23:365-74. Cai D.H., Wang D., Keefer J., Yeamans C., Hensley K., and Friedman A.D. (2008). C/EBPa:AP-1 leucine zipper heterodimers bind novel DNA element, activate the PU.1 promoter, and direct monocyte lineage commitment more potently Than C/EBPa homodimers or AP-1. Oncogene 27:2772-9. Zhang L., Fried F.B., Guo H., and Friedman A.D. (2008). Cyclin-dependent kinase phosphorylation of RUNX1/AML1 on three sites increases trans-activation potency and stimulates cell proliferation. Blood 111:1193-1200
CRB I, Rm. 253, 1650 Orleans St., Baltimore, MD 21231
(410) 955-2095
(410) 955-8897
Profile Page Photo: 
Alan D. Friedman, M.D.

Copyright ©2013 NHLBI Progenitor Cell Biology Consortium.

University of Maryland School of Medicine logo

National Heart Blood and Lung Institute logo