News and Events BMDCR
The BMDCR is pleased to announce the successful recruitment of Kay Macleod, Ph.D
Dr. Macleod received her Ph.D. in Pathology from the Beatson Institute for Cancer Research at the University of Glasgow, Scotland. Her thesis was completed under the mentorship of Dr. Mark Plumb and focused on the transcriptional regulation of erythroid-specific genes. Following a three-year postdoctoral fellowship in Dr. Dominique Stehelin's laboratory at the Pasteur Institute in France, Dr. Macleod joined Dr. Tyler Jacks' laboratory in the Massachusetts Institute of Technology Cancer Research Center. While in the Jacks lab, Dr. Macleod turned her attention to the role of the retinoblastoma tumor suppressor gene in cell proliferation, differentiation and programmed cell death using mouse models. Following her time at MIT, Dr. Macleod accepted a position as Instructor at the University of Dundee where she established the Transgenic Mouse Facility at Ninewells Hospital and Medical School at the University of Dundee. After several years in Dundee, Dr. Macleod now joins the Ben May at the rank of Assistant Professor.
Among Dr. Macleod's many honors are a Medical Research Council (UK) Studentship during her graduate work at the Beatson Institute, an INSERM International Research Fellowship and European Community Medical Research Prize during her time at the Pasteur Institute, and a Long-Term Fellowship from the Human Frontiers Science Program while at MIT.
In her research work, Dr. Macleod plans to focus her attention on the function of pRB in the hematopoietic system, where she has shown a critical role for pRb in regulating proliferation of erythroblasts. Loss of pRb in the mouse, either in the fetal liver or in the bone marrow of reconstituted mice, results in deregulated cell cycle of myeloid progenitors, a myeloproliferative disorder, anemia and death of the mouse. Despite this appreciation of the importance of Rb, we still do not have a molecular understanding of how pRb functions in the hematopoietic system. To address the molecular functions of the Rb tumor suppressor in hematopoiesis, Dr. Macleod proposes to carry out structure-function analysis in vivo and examine the altered activity of mutant forms of pRb in a primary erythroid cell culture system and in the mouse by gene targeting in embryonic stem cells. In the same way that understanding the effects of Rb loss in the central nervous system and lens established a paradigm for cooperation between Rb and p53 loss in tumorigenesis, Dr. Macleod believes it could be informative to assess whether any novel functions of Rb in hematopoiesis are relevant to an understanding of cancer progression.