LaMonica V. Stewart, Ph.D.
Assistant Professor
Department of Cancer Biology, Department of Biomedical Sciences

(615) 327-6749
West Basic Science Bldg., Rooms 2118/2120
1005 Dr. D.B. Todd Boulevard
Nashville, TN  37208

lstewart@mmc.edu

Lab URL

CV or Bio (PDF)

B.S., Biochemistry, Texas A&M University
Ph.D., Pharmacology and Toxicology, University of Texas Medical Branch

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.

Stewart LV, Lyles B, Lin MF, Weigel NL.  Vitamin D receptor agonists induce prostatic acid phosphatase to reduce cell growth and HER-2 signaling in LNCaP-derived human prostate cancer cells.  J Steroid Biochem Mol Biol. 2005 ;97:37-46.

Stewart LV, Weigel NL.  Role of insulin-like growth factor binding proteins in 1alpha,25-dihydroxyvitamin D(3)-induced growth inhibition of human prostate cancer cells.  Prostate. 2005;64:9-19.

Swamy N, Chen TC, Peleg S, Dhawan P, Christakos S, Stewart LV, Weigel NL, Mehta RG, Holick MF, Ray R.  Inhibition of proliferation and induction of apoptosis by 25-hydroxyvitamin D3-3beta-(2)-Bromoacetate, a nontoxic and vitamin D receptor-alkylating analog of 25-hydroxyvitamin D3 in prostate cancer cells.  Clin Cancer Res. 2004;10:8018-27.

Stewart LV, Weigel NL.  Vitamin D and prostate cancer. Exp Biol Med. 2004;229:277-84. Review.

Stewart LV, Song K, Hsing AY, Danielpour D.  Regulation of trespin expression by modulators of cell growth, differentiation, and apoptosis in prostatic epithelial cells. Exp Cell Res. 2003; 284:303-15.