Return to Faculty ListingMichael Henry Ph.D.
michael-henry
Professor of Molecular Physiology & Biophysics
Selected Publications
Drake, J.M., Gabriel, C L. and Henry, M.D. Assessing tumor growth and distribution in a model of prostate cancer metastasis using bioluminescence imaging. Clin. Exp. Metastasis, 2006 May 16; [Epub ahead of print]. Henry, M.D., Silva, M.D., Wen, S., Siebert, E. Solin, E., Chandra, S., Worland, P.J. Spiculated periosteal response induced by intraosseous injection of 22Rv1 prostate cancer cells resembles subset of bone metastases in prostate cancer patients. Prostate, 65:347-354, 2005. Henry, M.D., Wen, S., Silva, M., Chandra, S. Milton, M and Worland, P.J. (2004) A PSMA-targeted monoclonal antibody-chemotherapeutic conjugate designed for the treatment of prostate cancer. (Manuscript submitted). Cohn, R.D., Henry, M.D., Barresi, R., Saito, F., Flanagan, J.D., Moore, S.A., Skwarchuk, M.W., Robbins, M.E., Kahn, C.R., Williamson, R.W., and Campbell, K.P. (2002) Disruption of Dag1 in differentiated skeletal muscle reveals a role for dystroglycan in muscle regeneration. Cell, 110:639-648. Henry, M.D., Cohen, M.B., and Campbell, K.P. (2001) Reduced expression of dystroglycan in breast and prostate cancer. Hum. Pathology 32:791-795. |

Research in our laboratory is aimed at understanding the molecular and cellular biology underlying cancer metastasis. Dissemination of cancer cells from a primary tumor and survival and proliferation of those cells at a secondary site, metastasis, is viewed a complex multi-step process. Understanding this process is both fundamentally interesting as it involves basic biological mechanisms, such as intracellular signaling, cell-cell and cell-matrix interactions, and a critical exercise in medicine as metastasis is the predominant factor in the morbidity and mortality associated with cancer. To address questions about tumor metastasis, we utilize various mouse models, in vivo imaging technology and functional genomics. Among the questions we are seeking to understand with these combined approaches are why many cancers display different organ-site preferences for metastasis and why disseminated metastases apparently remain dormant for a period of time before growing aggressively. While at Millennium Pharmaceuticals, my laboratory developed models for metastatic colonization of various organs, including lung, liver and bone, utilizing bioluminescence imaging for visualizing tumor growth and dissemination in living animals. One such model that we have developed has features of clinical prostate cancer metastasis. As an initial focus of my research program, we are using this model to probe the cellular and molecular biology of prostate cancer metastasis with the goal of identifying molecules and mechanisms that underlie this condition.