Research in the laboratory of Peter Storz, Ph.D., focuses on the protein kinase D (PKD) family of serine/threonine kinases. Specifically, Dr. Storz's laboratory is interested in the mechanisms by which PKD is activated and how it relays signaling to regulate tumor development, tumor cell survival and tumor cell motility.
In breast cancer, Dr. Storz and his colleagues focus on the role of PKD in regulating the invasiveness and metastasis of cells. In pancreatic cancer, they focus on the role of reactive oxygen species and PKD in the regulation of events that initiate the development of this cancer.
- PKD as a regulator of actin reorganization and cell migration. During early metastatic events, reorganization of the actin cytoskeleton must occur to allow for tumor cell migration and invasion. Dr. Storz's laboratory has shown that PKD is a key enzyme regulating actin remodeling at the leading edge of migrating cells. Ongoing work aims to identify PKD substrates and test how their phosphorylation by PKD1 transfers to altered actin reorganization and cell motility.
- Role of PKD in invasive breast cancer. Current statistics for breast cancer show that survival could be significantly increased with better and earlier diagnosis of patients who are at risk of malignant progression. With PKD1, Dr. Storz's laboratory has identified a kinase that is downregulated in its expression in more than 90 percent of human invasive ductal carcinomas. Recent work indicates that PKD1 is a molecular switch that acts as a suppressor of breast tumor cell invasion.
- Reactive oxygen species (ROS) in aging and cancer. ROS contribute to cellular and organismal aging, senescence or cancer progression. Mitochondria are known to generate ROS in response to many stressors, and mitochondrial dysfunction is a common phenotype in cancer. Dr. Storz's laboratory has shown that in cancer cells, when cellular ROS increase, PKD localizes to the mitochondria, where it is activated and signals to the nucleus. Dr. Storz's research on this topic focuses on determining activators and targets for PKD in this signaling pathway.
- Acinar-to-ductal metaplasia (ADM) as a cause for pancreatic disease. After tissue injury or inflammation, pancreatic acinar cells undergo reprogramming that induces their transdifferentiation to a premature, duct-like phenotype. Cells that underwent ADM can progress to develop pancreatic intraepithelial neoplasia and eventually pancreatic cancer. Dr. Storz's current focus is on understanding the mechanisms that drive such reprogramming of primary pancreatic acinar cells.
Significance to patient care
Research on breast cancer in Dr. Storz's laboratory focuses on how PKD regulates cell motility and invasiveness and how this knowledge can be translated to develop strategies and tools for early detection and treatment of metastatic breast cancer.
The laboratory's research on pancreatic cancer focuses on how PKD contributes to the development and progression of this cancer, as well as on the development of tools for early detection and strategies for treatment.
- Member, Scientific Review Committee, Pancreatic Cancer Action Network-AACR Pathway to Leadership Grants, 2012
- Member, Pancreatic Cancer-2 Panel, Peer-Reviewed Cancer Research Program Discovery Award, Department of Defense, 2011
- Member, Editorial Board, ISRN Cell Biology, 2011
- Recipient, Pancreatic Cancer Action Network-AACR Career Development Award, 2008