Andrew J. Putnam
Chemical Engineering & Materials Science, The Henry Samueli School of Engineering Biomedical Engineering, The Henry Samueli School of Engineering
Phone: (949) 824-1243
Email: aputnam@uci.edu
http://cset.eng.uci.edu/
My Lab Home Page
http://www.faculty.uci.edu/profile.cfm?faculty_id=5104
HSSoE Faculty Profile
Andrew Putnam
Dr. Putnam’s primary research interest involves the extracellular matrix (ECM). Specifically, his lab is focused on understanding the structural/mechanical role of the ECM on cell function. The ultimate goal is to exploit their quantitative and predictive understanding of cell–ECM interactions to create novel biomaterial systems that mimic native ECM. They then hope to utilize these materials for tissue engineering applications and as in vitro models of various pathologies. Because cell-ECM interactions are often disrupted in tumorigenesis and metastasis, the lab is also very interested in these interactions in numerous human cancers as well.
With respect to cancer-related research, the primary interest is tumor cell migration and invasion. Tumor growth and invasion have been studied extensively both in vivo and in vitro. However, in vivo model systems can be plagued by an inability to control the growth environment, are typically very expensive, and are not easily conducive to analysis at the molecular level. On the contrary, in vitro cell culture systems permit the investigation of specific variables in a controlled fashion, yet in most cases these systems involve cell culture on flat, two-dimensional surfaces. Two-dimensional surfaces do not account for structural cues inherent in the tumor microenvironment that may provide permissive signals that allow tumor formation, growth, and metastatic spread that affect the functional behavior of tumors in the body.
In order to study tumor biology in an in vitro micro-environment that more closely mimics that found in the body, they have developed a model of skin cancer progression centered around a fibrin-based ECM. Adding small amounts of collagen to the model creates a collagen-fibrin composite ECM that more accurately mimics the tumor microenvironment in vivo. Current experiments are focused on correlating how the structural/mechanical properties of this model influence the 3-D invasion of metastatic and non-metastatic melanoma cells. They are also addressing the role of numerous integrin-mediated signal transduction pathways in this model system.
Selected Publications:
Lee, C. C., Putnam, A. J., Miranti, C. K., Gustafson, M., Wang, L. M., Vande Woude, G. F., and Gao, C. F. (2004). Overexpression of sprouty 2 inhibits HGF/SF-mediated cell growth, invasion, migration, and cytokinesis. Oncogene 23(30), 5193-202.
Ghajar, C. M., Suresh, V., Peyton, S. R., Raub, C. B., Meyskens, F. L., Jr., George, S. C., and Putnam, A. J. (2007). A novel three-dimensional model to quantify metastatic melanoma invasion. Mol Cancer Ther 6(2), 552-61.
Peyton, S. R., Kim, P. D., Ghajar, C. M., Seliktar, D., and Putnam, A. J. (2008). The effects of matrix stiffness and RhoA on the phenotypic plasticity of smooth muscle cells in a 3-D biosynthetic hydrogel system. Biomaterials 29(17), 2597-607.
Ghajar, C. M., Chen, X., Harris, J. W., Suresh, V., Hughes, C. C., Jeon, N. L., Putnam, A. J., and George, S. C. (2008). The effect of matrix density on the regulation of 3-D capillary morphogenesis. Biophys J 94(5), 1930-41. |
