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O.M. Zack Howard, Ph.D.

Portait Photo of O.M. Zack Howard
Laboratory of Molecular Immunoregulation
Cellular Immunology Group
Associate Scientist
Center for Cancer Research
National Cancer Institute
Building 560, Room 31-19
P.O. Box B
Frederick, MD 27102-1201
Phone:  
301-846-1348
Fax:  
301-846-6789
E-Mail:  
howardz@mail.nih.gov

Biography

Dr. Howard graduated for the University of Oklahoma in 1983 with a B.S. in chemistry and earned a Ph.D. in biochemistry from the University of South Carolina in 1987 with a Ph.D. dissertation entitled 'Determination of the primary structure of the subunit of human complement protein C8'. Following graduate school, Dr. Howard joined the University of Texas MD Anderson Cancer Center Molecular Hematology Program moving quickly from postdoctoral fellow to Project Investigator. While at the UT-MD Anderson Cancer Center Dr. Howard investigated the molecular escape of chronic myelogenous leukemia (CML) cells from interferon mediated growth suppression. In 1989, Dr. Howard moved to the National Cancer Institute-Frederick where she has remained. During her time with the NCI-Frederick, Dr. Howard has investigated the molecular regulation of growth factor receptors, IL-2Rbeta, prolactin receptor, the roles of chemokines and their receptors in cell migration, tumor metastasis and proliferation. Her most recent studies have included microRNA involved in regulating myeloid derived suppressor cells (MDSC) and cancer-pain signal cascades through TRPV1.

Research

Dr Howard's recent work has shown that endogenous proteins or self-antigens can attract specialized white blood cells and they use chemokine receptors, which are a subset of G-protein coupled receptors (GPCRs also known as 7-transmembrane receptors) to mediate their effects. However, these self-antigens, which are also known as autoantigens and tumor antigens, are not structurally related to chemokines and appear to differ from chemokines in that they may associate with different domains of the receptor and activate different receptor mediated signaling. What makes tumor-antigens unique is that they appear to compel immune cells behave as immune suppressors. Currently, Dr. Howard is characterizing suppressive myeloid cells induced by tumor antigens using phenotypic and functional assays. Her studies of suppressive myeloid cells are expanding to include microRNA and signal cascades essential for suppressive cell activity.

This page was last updated on 3/24/2014.