Stem Cell Biology + CML
Myrtle Gordon’s current research is focused on the investigation of chronic myeloid leukaemia (CML) and normal haemopoietic stem cell kinetics. Her group was the first to demonstrate, in 1987, that progenitor cells in CML are defective in their ability to bind to bone marrow-derived stromal cells, providing an explanation for the circulation of numerous CML progenitor cells. More recently, they have found that CML progenitors have an increased capacity for self-renewal in vitro and that interferon-alpha could correct this defect. They have also discovered that normal, but not CML, progenitor cells bind together and transmit an antiproliferative signal to one another through mutually expressed CD34.
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Definition of links between molecular defects and cell kinetics in CML
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The cellular basis for therapy in CML
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Mechanisms controlling the kinetics of haemopoietic stem and progenitor cell self-renewal (including cytokines, chemokines, oncogenes, cell cycle proteins and extracellular matrix proteins)
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The role of CD34-mediated homotypic progenitor cell adhesion in the regulation of normal haemopoiesis and in CML
Cells bound by interaction of cell surface CD34 (green fluorescence)
