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Alan David Friedman, M.D.

Photo of Dr. Alan David Friedman, M.D.

King Fahd Professor of Pediatric Oncology

Professor of Oncology

Male

Expertise: Acute Lymphoblastic Leukemia (ALL), Acute Myeloid Leukemia (AML), Chronic Myeloid Leukemia (CML), General Pediatrics, Germ Cell Tumors, Hodgkin's Disease, Leukemia, Medical Oncology, Myelodysplastic Syndromes (MDS), Non-Hodgkin's Lymphoma (NHL), Pediatric Oncology, Retinoblastoma, Wilms Tumor ...read more

Research Interests: Regulation of Myeloid Differentiation and Transformation

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Locations

The Johns Hopkins Hospital (Main Entrance)
Appointment Phone: 410-955-8751

1800 Orleans St.
The Charlotte R. Bloomberg Children's Center Building, 11th Floor
Baltimore, MD 21287 map
Fax: 410-955-8897

Background

Dr. Friedman is the King Fahd Professor of Oncology and Professor of Pediatrics at the Johns Hopkins University School of Medicine and a member of the Johns Hopkins Kimmel Cancer Center. He received his M.D. from the Harvard Medical School (1983), did his pediatric internship and residency at Boston Children's Hospital (1983-86), and completed a fellowship in pediatric hematology-oncology at Johns Hopkins (1986-89). As a fellow, he did post-doctoral research at the Carnegie Institution Department of Embryology located on the Johns Hopkins Homewood campus. Dr. Friedman has served on the Pediatric Oncology faculty at Johns Hopkins since 1989. His laboratory focuses on investigation of normal and abnormal blood-cell formation. Dr. Friedman also cares for children with cancer, specializing in the treatment of leukemia.

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Titles

  • King Fahd Professor of Pediatric Oncology
  • Professor of Oncology
  • Professor of Pediatrics

Education

Degrees

  • MD, Harvard Medical School (1983)

Residencies

  • Children's Hospital / Pediatrics (1986)

Fellowships

  • Johns Hopkins University School of Medicine / Pediatric Hematology & Oncology (1989)

Board Certifications

  • American Board of Pediatrics / Pediatric Hematology-Oncology (1990, 2005)
  • American Board of Pediatrics / Pediatrics (1987)

Research & Publications

Research Summary

RUNX1 is a transcription factor required for the formation of the hematopoietic stem cell (HSC) and for its further maturation. RUNX1 is commonly mutated or involved in chromosomal translocations associated with AML or ALL. Dr. Friedman''s laboratory is investigating the mechanisms that allow RUNX1 to regulate normal hematopoietic stem cells and myeloid differentiation and to stimulate cell cycle progression. He ultimately envisions developing means to manipulate RUNX1 to assist formation and expansion of HSC from embryonic stem cells and to assist formation of autologous neutrophils to benefit patients with neutropenia. In addition, Dr. Friedman is investigating how mutations of RUNX1 or its partner CBFb contribute to acute leukemia, focusing on CBFb-SMMHC, a fusion oncoprotein expressed from the inv(16) chromosome in a subset of AML patients. Ultimately, he would like to identify small molecules that target CBFb-SMMHC to assist in the therapy of AML.

C/EBPa is a transcription factor required for formation of normal neutrophils and monocytes. C/EBPa is also commonly mutated in blasts derived from patients with AML. Dr. Friedman''s laboratory is investigating how C/EBPa cooperates with other proteins, including cytokines such as G-CSF or M-CSF, to control normal myeloid development. In addition, he is investigating how mutant forms of C/EBPa contribute to AML, in particular focusing on how interaction between C/EBPa and another transcription factor, NF-kB, inhibits apoptosis. By mapping the amino acids through which these proteins interact, Dr. Friedman hopes to ultimately design small molecules that prevent their interaction to induce leukemic cell death and contribute to the therapy of AML. As C/EBPs and NF-kB are also expressed also in other malignancies and in inflammatory cells which contribute to cancer formation and progression, such a small molecule might in addition have broader utility as a novel therapeutic.

Lab

Dr. Friedman investigates 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). In conducting these studies he focuses on two proteins, RUNX1 and C/EBPa, which regulate normal bone marrow development but are also commonly mutated in AML. Dr. Friedman is attempting to build on his basic research to develop useful clinical applications. In particular, he is pursuing small molecules that interfere with the action of leukemic RUNX1 or C/EBPa proteins as potential novel therapies for AML, and he is investigating means to expand normal blood stem cells to benefit patients with marrow failure or those many patients receiving chemotherapy who would benefit from blood product support to avoid anemia, bleeding, and infections.

Selected Publications

Nuchprayoon I, Meyers S, Scott LM, Suzow J, Hiebert S, Friedman AD. PEBP2/CBF, The Murine Homolog of the Human Myeloid Proto-oncogenes AML1 and PEBP2/CBF, Regulates the Murine Myeloperoxidase and Neutrophil Elastase Genes in Immature Myeloid Cells. Mol. Cell. Biol. 1994; 14(8):5558-68.

Kummalue T, Lou J, Friedman AD. Multimerization via its Myosin Domain is a Prerequisite for Inhibition of CBF Activities by the CBF-SMMHC Myeloid Leukemia Oncoprotein. Mol. Cell. Biol. 2002; 22(23):8278-91.

Cai DH, Wang D, Keefer J, Yeamans C, Hensley K, Friedman AD. C/EBP:AP-1 Leucine Zipper Heterodimers Bind Novel DNA Element, Activate the PU.1 Promoter, and Direct Monocyte Lineage Commitment More Potently Than C/EBP Homodimers or AP-1.Oncogene 2008; 27(19):2772-9.

Leong WY, Guo H, Ma O, Huang H, Cantor AB, Friedman AD. Runx1 Phosphorylation by Src Increases Trans-Activation via Augmented Stability, Reduced Histone Deacetylase (HDAC) Binding, and Increased DNA Affinity, and Activated Runx1 Favors Granulopoiesis. J. Biol. Chem. 2016; 291(2):826-36.

Guo H, Cooper S, Friedman AD. In Vivo Deletion of the +37 kb Cebpa Enhancer Markedly Reduces Cebpa mRNA in Myeloid Progenitors but Not in Non-Hematopoietic Tissues to Impair Granulopoiesis. PLoS One 2016; 11(3):e0150809.

Activities & Honors

Honors

  • Biochemistry Department Award, University of California, Berkeley, 1979
  • cum laude, Harvard Medical School, 1983
  • Searle Scholar Award, Chicago Community Trust, 1991 - 1996
  • Scholar Award, Leukemia and Lymphoma Society, 1998 - 2003
  • Stohlman Scholar, Leukemia and Lymphoma Society, 2003
  • Oncology Center Director's Teaching Award in Basic Science, Johns Hopkins University, 2004

Memberships

  • American Academy of Pediatrics, 1996
  • American Association for the Advancement of Science, 1990
  • American Society of Hematology, 1994
  • American Society of Pediatric Hematology-Oncology, 1994
  • Pediatric Oncology Group/Children''s Oncology Group, 1989
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