Steven M. Hill, Ph.D.
Edmond & Lily Safra Chair for Breast Cancer Research
Tulane Cancer Center Program Member
Address: 1430 Tulane Ave., SL-49, New Orleans, LA 70112
Dr. Hill received his B.S. in Biology from Abilene Christian University in 1980. He conducted his doctoral studies on the cellular mechanisms of the pineal hormone on growth of human breast cancer under the tutelage of Dr. David E. Blask at the University of Arizona, obtaining his Ph.D. in 1986. From 1986 to 1988 Dr. Hill was a postdoctoral fellow with the late Dr. William L. McGuire at the University of Texas Medical Center at San Antonio, working on the molecular mechanisms of estrogen-resistance in human breast cancer. In 1988 Dr. Hill returned to Abilene Christian University where he taught Anatomy/Physiololgy, Cell Biology, and Developmental Biology. In 1989 Dr. Hill joined Tulane University Health Sciences Center in the Department of Structural and Cellular Biology, where he is the course director for Medical Embryology. Dr. Hill has published over 60 manuscripts and book chapters in the area of molecular endocrinology and breast cancer. He is a reviewer for a variety of journals including Cancer Research, Breast Cancer Research and Treatment, and Molecular Endocrinology and has served on NIH, DOD, and NSF grant review panels. The primary focus of Dr. Hill's research is the molecular mechanisms of signal transduction cross- talk in breast cancer. Breast cancer is an endocrine-responsive neoplasm and as such is responsive to a variety of endocrine and growth factor stimuli. A complete understanding of the factors regulating the proliferation breast cancer, as well as an understanding of how these various hormones and factors cross-talk with each other to regulate breast cancer cell growth, is crucial to development of more potent breast cancer therapies. Dr. Hill's laboratory has conducted extensive studies examining the role of mutated estrogen receptors in the development of an estrogen-insensitive/tamoxifen-resistant phenotype in breast cancer. They have identified variant forms of the estrogen receptor that can function independent of hormone stimulation and can act to constitutively drive the mitogenic estrogen-response pathway in breast cancer. More recently, Dr. Hill's laboratory has demonstrated that the pineal hormone melatonin has significant inhibitory effects on the development and growth of human breast cancer. Furthermore, their studies have elucidated that melatonin can potentiate the actions of retinoic acid, a vitamin A derivative, to induce cell death in human breast tumor cells in culture, to prevent the development of carcinogen-induced breast cancer in rats and to induce the regression of over 70% of established breast tumors in rats. These studies currently are being moved into human clinical trials. Finally, Dr. Hill, in collaboration with investigators at Tulane Cancer Center and Xavier University, is examining the cross-talk of signaling pathways such as the melatonin receptor with the retinoic acid receptor and estrogen-receptor in both breast and prostate cancer and how these pathways can be manipulated to provide enhanced therapeutic advantage.
Eck M, Yuan L, Duffy L, Ram PT, Ayettey S, Chen LL, Cohn CS, Reed JC, Hill SM. A sequential regimen of melatonin and all-trans retinoic acid induces apoptosis in Human Breast tumor cells. Br J Cancer 77: 2129-2137 (1998)
Ram PT, Kiefer T, Silverman M, Song Y, Brown GM, Hill SM. Estrogen receptor transactivation in MCF-7 breast cancer cells by melatonin and growth fractors. Mol Cell Endocrinol 141: 53-64 (1998)
Hill SM, Teplitzky S, Ram PT, Kiefer T, Blask DE, Spriggs LL, Eck KE. Melatonin synergizes with retinoic acid in the prevention and regression of breast cancer. Adv Exp Med Biol 460: 345-62 (1999)
Dai J, Kiefer T, Yuan L, Hill SM. Retinoid orphan receptor-alpha expression in human breast cancer and modulation of their transcriptional activity by the pineal hormone melatonin. Mol Cell Endorinol 176:111-120 (2001)
Jones FE, Burow ME, Hill SM. Signal transduction in breast cancer: silencing the cross-talk. Eur Biopharmaceut Rev 70-73 (2003)