Scott D. Cramer, Ph.D., Associate Professor
Dr. Cramer received his B.A. from the University of California in Santa Cruz in 1984 and his Ph.D. from the same university in 1992. He had a post-doctoral fellowship at Stanford University School of Medicine from 1992 - 1996.

SYNOPSIS OF AREA OF INTEREST:: The current focus of his research is on the molecular dissection of signaling pathways in prostatic cells, the identification of prostate progenitor or stem cells, and understanding epithelial-stromal interactions in normal and abnormal ductal morphogenesis. The three systems are highly integrated both conceptually and programmatically.

DETAILED AREA OF INTEREST: Signaling: Previously published studies have used genetic models for investigating the signaling pathways involved in vitamin D growth inhibition and also have demonstrated strong synergistic growth inhibition between vitamin D and genistein on prostatic cells. In addition, his lab's data demonstrate that vitamin D and genistein cooperatively induce p21 proteinand that genistein upregulates vitamin D receptor (VDR) content by modulating protein stability. The effect of genistein on VDR content leads to the hypothesis that one mechanism of synergism between vitamin D and genistein is by enhanced VDR signaling. Stem Cells: They are developing techniques to isolate cells from the prostate with stem-cell like properties. The lab team has developed an in vitro 3-dimensional culture system and are currently evaluating the effects of different culture conditions on ductal morphogenesis and differentiation. Their goal is to make fully functional prostatic structures in vitro using defined medium. Epithelial Stromal Interactions: The development of normal and abnormal glandular structures in the prostate is controlled at the endocrine and paracrine levels by reciprocal interactions between epithelium and stroma. His group has developed a method of fresh human prostate tissue acquisition for reproducible isolation of cells from defined histologies and have demonstrated fundamental differences in the inductive capabilities of stromal cells derived from normal or diseased prostatic tissue. Normal stromal cells have no apparent ability to induce epithelial cell growth in a prostate recombination model. Stromal cells derived from benign prostatic hyperplasia induce sharply circumscribed structures. The results support a growing body of work demonstrating that the tumor microenvironment, and specifically, epithelial-mesenchymal interactions are critically important for tumorigenesis. These studies argue that more focused attention should be directed towards the nature of cancer associated stroma. To this end Dr. Cramer and his colleagues plan to compare expression profiles of the normal, BPH and cancer stromal cells to identify candidates for further study using their genetically defined systems.

PUBLICATIONS:

Barclay WW, Woodruff RD, Hall MC, Cramer SD. 2005 A system for studying epithelial-stromal interactions reveals distinct inductive abilities of stromal cells from benign prostatic hyperplasia and prostate cancer. Endocrinol: 146: 13-18.

Rao A, Coan A, Welsh J-E, Barclay WW, Koumenis C, Cramer SD. 2004 vitamin D receptor and p21/waf1 are targets of genistein and 1,25-dihydroxyvitamin D3 in human prostate cancer cells. Can Res: 64:2143-2147.

Cramer SD, Chang B-L, Rao A, Hawkins GA, Zheng SL, Wade WN, Cooke R, Thomas LN, Bleeker ER, Catalona WJ, Sterling DA, Meyers DA, Ohar J, Xu J. 2003 Association between genetic polymorphism in the prostate-specific antigen gene promoter and serum prostate-specific antigen levels. J Nat Can Inst: 95(14):1044-1053.

Rao A, Chang B-L, Hawkins G, Hu JJ, Rosser CJ, Hall, MC, Meyers DA, Xu JF, Cramer SD. 2003 Analysis of the G/A polymorphism in the androgen response element I of the PSA gene and its interactions with androgen receptor polymorphisms. Urol:61:864-869.

Wade WN, Kute T. Koumenis C, Willingham MC, Cramer SD. 2002 p27Kip1 is essential for the antiproliferative action of 1,25-dihydroxyvitamin D3 in primary but not immortalized mouse fibroblasts. J Biol Chem: 277:37301-37306.

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