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The Tumor Promoting Role of BAD in Breast Cancer Cells Open Access


Other title
tumor growth
breast cancer
Type of item
Degree grantor
University of Alberta
Author or creator
Buckland, Timothy, W
Supervisor and department
Goping, Ing Swie (Biochemistry)
Examining committee member and department
Godbout, Roseline (Oncology)
Fahlman, Richard (Biochemistry)
Goping, Ing Swie (Biochemistry)
Baksh, Shairaz (Pediatrics)
Department of Biochemistry

Date accepted
Graduation date
Master of Science
Degree level
In Canada, approximately 40% of the population will be diagnosed with cancer and 25% will die of this disease. In order to treat cancer more effectively, new prognostic and therapeutic targets need to be discovered. In breast cancer, the BH3 only protein BAD has been shown to correlate with response to treatment. However, the role of BAD in cancer is unclear. Although BAD is well characterized as a pro-apoptotic protein, alternative roles exist that may influence cancer progression. In this study, we determine that BAD over-expression promotes proliferation and tumor growth of MDA-MB-231 breast cancer cells. These roles are regulated by serine phosphorylation, specifically serine 118. Finally, enforced phosphorylation of BAD at serine 118 promotes apoptotic resistance. This study suggests that in order to use BAD as a prognostic or therapeutic target, the phospho-status of BAD must also be examined.
Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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