The study findings were published recently in The Journal of Biological Chemistry http://www.jbc.org/cgi/reprint/282/26/19122.
The team can use the results of this kind of disruption of normal km23 function for clues about what might happen to the protein in ovarian cancer cells. Then, drug development, targeting the irregular function of the protein, can begin.
Our studies provide a better understanding of how the protein works, what it does, and how its functions may be altered in cancer cells. This leads us to the critical next step -- the design of drugs that can repair the defect in the cancer cells without interrupting the processes of the normal cell, Mulder said. When you find something that isnt working right in the cancer cells, it suggests possibilities as to how to intervene to fix the problem.
Epithelial ovarian cancer is often diagnosed at an advanced stage and accounts for about 15,000 deaths each year. Despite advances in surgical techniques and chemotherapy, overall survival rates have not improved significantly because of late detection, often after the disease has already spread to remote organs. Identification of an early warning signal and a new therapeutic agent for the disease should lead to improved survival rates.