Stromal-Epithelial Interactions in Prostate Cancer Bone Metastases

The laboratory is investigating the mechanism underlying the predilection of prostate cancer to metastasize to bone and induce an osteoblastic reaction. In studies funded by the Department of Defense, we have uncovered a role for cyclo-oxygenase-2 (COX-2) and PGE2 in these processes. In addition, we have reported that androgens target bone osteoblasts and, via induction of canonical Wnt signaling, enhance the growth of prostate cancer cells in the bone environment. These studies are being carried out in collaboration with Dr. Stuart Aaronson’s laboratory who have been providing many of the reagents and vectors needed to study canonical Wnt signaling.

Prostate Cancer Stem Cells

Ongoing funded studies have been investigating our hypothesis that increased ratios of estrogens/androgens in males impairs normal prostate differentiation and may lead to the development of prostate cancer. In collaboration with the laboratories of Drs. Friedman, Martignetti, and Narla, we are determining whether steroid hormone effects on prostate epithelial cell differentiation are mediated by effects on the known prostate cancer tumor suppressor protein, KLF6.