Stephen T. Sawyer, Ph.D. Professor and Graduate Program Director 1112 East Clay Street McGuire Hall Room 100F P.O. Box 980613 Richmond, Virginia 23298-0613 Phone: (804) 828-7918 E-mail: ssawyer@vcu.edu Publications: selected | PubMed

Education: University of Tennesee, 1980

Research interests:

The National Institutes of Health has funded the laboratory since 1987 to study erythroid cell biology and the abnormal signals that arise in leukemia. In the past, our work was primarily been directed to the study of erythropoietin (EPO, the hormone that regulates red blood cell formation) and the EPO receptor. The scope of research has now widened to encompass the study of intracellular signaling activated by EPO and other hematopoietic growth factors such as stem cell factor (SCF) that control proliferation, differentiation, survival and progression to apoptosis (programmed cell death) of erythroid and leukemic cells. Research in the following areas of study is either under way or planned:

Apoptosis/programmed cell death research

• Cell signaling pathways that activate phosphorylation of the Bcl family protein, Bad, that modulates survival
• Regulation of Bcl-Xl expression that maintains survival
• Modulation of PI3-kinase by EPO and SCF and mechanisms for constitutive PI3-kinase activity in leukemic cells
• Role of JunB expression as a trigger of apoptosis or programmed cell death
• Ratio of expression of Bcl-Xl to Bad as a survival factor for leukemic cells

Proliferation/differentiation research

• Role of tumor necrosis factor-alpha as autocrine stimulator of proliferation
• Mechanism by which stem cell factor triggers proliferation without protection from apoptosis
• Mechanism by which over-expression of JunB directs erythroid differentiation
• Effects of cannabinoids on proliferation

Erythropoietin receptor research

• What is the role of phosphorylation of the EPO receptor (EPOR) at both serine and tyrosine residues?
• Why does JAK2 kinase selectively interact with only a modified subset of EPO receptors?
• What is the role of ubiquitination of EPOR?

Selected publications:

Abutin RM, Chen J, Lung TK, Lloyd JA, Sawyer ST, and Harada H. (2009) Erythropoietin-induced phosphorylation/degradation of BIM contributes to survival of erythroid cells. Exp Hematol. 37(2):151-8.

Gewirtz DA, Di X, Walker TD, and Sawyer ST. (2006) Erythropoietin fails to interfere with the antiproliferative and cytotoxic effects of antitumor drugs. Clin Cancer Res. 12(7 Pt 1):2232-8.

Chen J, Jacobs-Helber SM, Barber DL, and Sawyer ST. (2004) Erythropoietin-dependent autocrine secretion of tumor necrosis factor-alpha in hematopoietic cells modulates proliferation via MAP kinase--ERK-1/2 and does not require tyrosine docking sites in the EPO receptor. Exp Cell Res. 2004 Aug 1;298(1):155-66.

Jacobs-Helber SM, Sawyer ST. (2004) Jun N-terminal kinase promotes proliferation of immature erythroid cells and erythropoietin-dependent cell lines. Blood. 104(3):696-703.

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