| LaMonica V. Stewart, Ph.D. |
| Assistant Professor Department of Cancer Biology, Department of Biomedical Sciences West Basic Science Bldg., Rooms 2118/2120 1005 Dr. D.B. Todd Boulevard Nashville, TN 37208 Phone: (615) 327-6749 |
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| The research in Dr. Stewart’s laboratory focuses on the compounds that activate the peroxisome proliferator activated receptor gamma (PPARγ) The research in Dr. Stewart’s laboratory focuses on the compounds that activate the peroxisome proliferator activated receptor gamma (PPARγ) have been shown to reduce growth of cultured human prostate cancer cells in vitro as well as prostate tumors in mouse models of prostate cancer. They are investigating the mechanisms that underlie PPARγ ligand-induced growth inhibition, that make it difficult to identify patients that would benefit from therapies involving PPARg ligands. The research goal of their laboratory is to further define the pathways by which PPARγ ligands reduce human prostate tumor growth and progression. They are currently using human prostate cancer cell lines and athymic mouse xenograft models to define the signaling pathways that mediate PPARγ ligand-induced alterations in prostate cancer gene expression and cell proliferation. In addition, they are conducting studies to determine whether PPARγ ligands decrease cancer cell invasion and other processes required for the formation of prostate cancer metastases, with the ultimate goal of developing new therapies to decrease the spread of both early and late-stage prostate cancer. ) have been shown to reduce growth of cultured human prostate cancer cells in vitro as well as prostate tumors in mouse models of prostate cancer. They are investigating the mechanisms that underlie PPARγ ligand-induced growth inhibition, that make it difficult to identify patients that would benefit from therapies involving PPARγ ligands. The research goal of their laboratory is to further define the pathways by which PPARϒ ligands reduce human prostate tumor growth and progression. They are currently using human prostate cancer cell lines and athymic mouse xenograft models to define the signaling pathways that mediate PPARγ ligand-induced alterations in prostate cancer gene expression and cell proliferation. In addition, they are conducting studies to determine whether PPARγ ligands decrease cancer cell invasion and other processes required for the formation of prostate cancer metastases, with the ultimate goal of developing new therapies to decrease the spread of both early and late-stage prostate cancer. | ||||||||||||||||
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© 2009 Meharry Medical College
1005 Dr. D.B. Todd Jr., Blvd.
Nashville, TN, 37208
(615) 327-6111
Last Updated: April 25, 2011
