J. Thomas Parsons
- BA, Chemistry, Depauw University, Greencastle, IN
- PhD, Biochemistry, Duke University, Durham, NC
- Postdoc, DNA Tumor Virology, St. Louis University, St Louis, MO
- Postdoc, RNA Tumor Virology, Universitat Zurich, Zurich, Switzerland
Adhesion Signaling in Normal, Cardiovascular and Cancer Cells
For the past 25 years my laboratory has been interested in how the activation of protein tyrosine kinases contributes to cancer progression and metastasis. In 1991 we identified Focal Adhesion Kinase (FAK) as an integrin regulated tyrosine protein kinase and in the ensuing years identified and characterized the signaling pathways regulated by adhesion to the extracellular matrix. Our studies have helped to define the role of FAK in tumor initiation, progression and metastasis and have laid ground work for efforts to develop small molecule inhibitors to FAK. We have helped to characterize one such inhibitor that has gone on to phase I trials in cancer patients. In the past 10 years my laboratory has focused on how receptor and non-receptor tyrosine kinase signaling contributes to tumor growth and metabolism and response to therapies, with particular interest in the tumor microenvironment. This interest has manifested itself in a highly productive and interactive collaboration with Todd Bauer, Associate Professor of Surgery and led to the establishment of patient-derived xenografts of pancreatic cancer as a model to develop effective combinatorial therapies for pancreatic adenocarcinomas. We have further developed mouse models that recapitulate the steps in the metastatic outgrowth of pancreas cancers in the liver. We are using these models to identify novel therapies for patients with recurrent metastatic disease.