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Education and Training:

B.A. in Biology/Classics
University of Pennsylvania Philadelphia, PA (1983)

M.D., Ph.D. (in Molecular and Cellular Pharmacology), State University of New York at Stony Brook, Stony Brook, NY (1992)

Residency in Internal Medicine, University of Maryland School of Medicine, Baltimore, MD (1992-95)

Chief Resident Physician, University of Maryland, Baltimore Veteran's Affairs Medical Center, Baltimore, MD (1995-96)

Fellowship in Hematology, University of Washington, Seattle, WA (1996-99)

Clinical Research Fellow, Fred Hutchinson Cancer Research Center, Seattle, WA (1999-2000)

Robert E. Richard, M.D., Ph.D.
Associate Professor of Medicine
Division of Hematology
University of Washington School of Medicine

Director, Hematology
VA Puget Sound Health Care System

Office Address:
VA Puget Sound Health Care System
S-111-Onc
1660 S. Columbian Way
Seattle, WA  98108

Phone:   (206) 277-1625
Fax:       (206) 764-2851
E-mail:    rrichard@u.washington.edu
Lab Website: http://faculty.washington.edu/rrichard/

 

CURRENT CLINICAL INTERESTS

I see patients with general hematological disorders at the VA on Tuesday afternoons.  I have a clinical interest in myeloproliferative disorders and other bone marrow disorders of the elderly.  In collaboration with Bill Hobbs of the Puget Sound Blood Center, I run an Adult Sickle Cell Clinic at the Seattle Cancer Care Alliance on the third Thursday afternoon of the month.


CURRENT RESEARCH INTERESTS


Research in novel methods in gene and cell therapy.


RESEARCH DESCRIPTION


Our research group is based at the Seattle Division of the VA Puget Sound Health Care System in the Beacon Hill neighborhood.

Pathogenesis of the classic myeloproliferative disorders.  The discovery of the role of the Jak2V617F mutation in myeloproliferative disorders (MPDs) helped explain the phenotype of this class of stem cell disorder.  Previous work performed in the lab of Tony Blau demonstrated the proliferative potential of a regulatable mpl molecule in human cells to expand human erythroid precursors.  However, with other growth promoting cytokines, other cell lineages could be expanded.  We believe that the pleiotropic effects of dysregulated Jak2 signaling in the MPDs is explained by activation of other gene pathways.  Using retroviral gene transfer of the MPD mutations we intend to identify other gene pathway that play a role in MPD pathogenesis.

Stem cell gene therapy to treat advanced HIV infection.  Treatment for HIV infection are continually changing in response to the appearance of strains resistant to standard medications.  Genetically engineered immune cells derived from adult blood stem cells could help rebuild the immune systems of AIDS patients.  We have developed retrovirus vectors that can enter human blood stem cells and genetically alter the stem cells so that all cells are protected from HIV infection.  By transplanting AIDS patients with genetically modified stem cells, an immune system protected from infection can develop.

The virus vectors we have developed are based on foamy virus, a non human primate virus that has never been associated with a specific disease.  A major advantage of this vector system is its ability to make virus particles in the presence of anti-HIV genes.  This is not the case with other vector systems in development for this purpose.  In fact, when expressed in a different vector based on lentiviruses, two of the genes in our anti-HIV vector block the ability to make the vector.  We have been able to high-titer stocks of our anti-HIV vector so that a clinical trial could be performed.  The results of our studies were published in Molecular Therapy in January 2008.  We are pursuing further studies in anticipation of submitting an investigational new drug application to the Federal Drug Administration.


SELECTED PUBLICATION

Richard RE, Wood B, Zeng H, Jin L, Papayannopoulou T, and Blau CA: Expansion of genetically modified primary human hemopoietic cells using chemical inducers of dimerization. Blood 95:430-6, 2000.

Richard RE, and Blau C: Small molecule directed Mpl signaling can complement growth factors to selectively expand genetically modified cord blood cells. Stem Cells 21:71-8, 2003.

Richard RE, Weinreich M, Chang KH, Ieremia J, Stevenson MM, Blau CA: Modulating erythrocyte chimerism in a mouse model of pyruvate kinase deficiency. Blood  103::4432-39, 2004.

Richard RE, de Claro RA, Chien S, Kiem HP, Clackson T, Andrews R, and Blau CA: CID-mediated in vivo selection: heterogeneity among large animal models. Molecular Therapy, 10(4):730-40, 2004.

Taylor JA, Vojtech L, Bahner I, Kohn DB, Laer DV, Russell DW, and Richard RE:  Foamy virus vectors expressing anti-HIV transgenes efficiently block HIV-1 replication.  Mol. Ther. 16:46-51, 2008.