Hello!
My name is Kyle Biggar and I am doing my PhD. in Molecular Biology at Carleton University, in Ottawa, Ontario. Throughout my undergraduate university education at St. Francis Xavier University (StFX), I had the opportunity to work with several professors in various laboratory settings. While completing these studies at StFX, I developed a keen interest in the field of anoxia tolerance and metabolic regulation. These unique interests, in the complexities of molecular biology, directed my studies to Dr. Kenneth Storey’s lab here in Ottawa, at Carleton University. While working in Dr. Storey’s lab, I have taken on many new and exciting projects. One such project examines the proliferation (growth and duplication) state of cells in hypoxic environments, not unlike that seen in hypoxic cores of tumours.
Extreme hypoxia is central to a variety of diseases including cardiac and pulmonary dysfunction as well as tumor progression. Recent insights into the molecular mechanisms of tumor growth have promised refined and effective cancer treatments. Although cancers are incredibly diverse, researchers have been searching for a small number of underlying controls, whose unregulated activity is required for the development of all cancers. Many of these studies examine cell cycle (the process of cellular growth and division) components as key players in the uncontrollable proliferation and the progression of tumor growth. Cell cycle regulation in hypoxic (low oxygen) environments, such as that of tumor cores, has shown great potential to expose the secrets of cell cycle arrest. Given this, there has been an overwhelming interest in the clarification of the molecular mechanisms regulating cell survival in various levels of oxygen deprivation. Many of these studies focus on hypoxia tolerant invertebrate models, failing to address the complexity of vertebrate systems (ie. Humans). Although the mechanisms of cell cycle arrest appear to be highly conserved throughout evolution, examination of an hypoxia tolerance vertebrate animal model may prove to be useful in elucidating the primary mechanisms of vertebrate cell cycle arrest in response to hypoxia.
Exciting stuff right? Stay tuned... I'll tell you more tomorrow :)
Monday, February 1, 2010
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