Bailey hypothesizes that, even before PanIN formation, activation of KRAS will fundamentally change pancreas cells, leading to increased growth and altered cellular characteristics. By studying the very earliest steps of pancreatic cancer development, Bailey's work can shed light on novel ways to detect or treat the disease, before it has progressed to a more aggressive stage.
Seeley works primarily in the laboratory of Maxence V. Nachury, Ph.D. Nachury was the recipient of the 2009 Pancreatic Cancer Action Network AACR Career Development Award, in memory of Larry Kwicinski. Nachury's funding period will expire as Seeley's begins, allowing seamless financial support for important pancreatic cancer research.
Seeley's project, Transport Proteins as Modifiers of Oncogenic Signaling in Pancreatic Cancer, represents efforts to define alternative strategies for limiting the effects of cancer-causing cellular signaling.
Transport proteins control the activities of proteins that cause cancer by positioning them either where they can promote cell growth or where they can be shut off. Seeley has found that a protein transport system called intraflagellar transport (IFT) determines the outcome of pancreatic cancer-causing mutations in mice. When the amount of IFT protein is decreased, the rate of pancreatic cancer formation in mice more than doubles. However, when IFT genes are completely missing, mice prone to pancreatic cancer develop only benign, non-lethal cysts. Fittingly, he finds that while decreases in IFT are frequent in human cases of pancreatic cancer, complete losses of IFT genes are very rare.
Because IFT is known to regulate the activities of several important cancer-causing signaling pathways by functioning in a cellular antenna known as the primary cilium, his findings suggest that
|Contact: Michele Sharp|
American Association for Cancer Research