References:
- Hyder, S. M., Murthy, L., and Stancel, G. M. Progestin regulation of vascular endothelial growth factor (VEGF) in human breast cancer cells. Cancer Res. 58:392-395, 1998.
- Hyder, S .M., Stancel, G. M., Chiappetta, C., Murthy, L., Boettger-Tong, H. L., and Makela, S. Uterine Expression of Vascular Endothelial Growth Factor (VEGF) is Increased by Estradiol and Tamoxifen. Cancer Res. 56: 3954-3960, 1996.
- Hyder S. M., Nawaz, Z., Chiappetta, C., Yokoyama, K., and Stancel, G. M. The Protooncogene c-jun Contains an Unusual Estrogen Inducible Enhancer within the Coding Sequence. J. Biol. Chem. 270:8506-8513, 1995.
George M. Stancel, Ph.D.
Dean, GSBS
UTHSC-Medical School, (713) 500 - 9880
George.M.Stancel@uth.tmc.edu
Estrogen control of cell proliferation
A major problem in cell biology is to elucidate the mechanisms by which diffusible molecules (hormones, autocoids, growth factors, neurotransmitters, etc.) regulate processes such as development, differentiation and proliferation of target organs. Steroid hormones provide some of the major model systems to study these processes, and our laboratory is specifically interested in the mechanisms by which hormones such as estradiol regulate target tissue growth and differentiation. For these studies we use the rodent uterus as a model of a normal estrogen target tissue. This is an ideal system since the uterine response to estrogens is rapid, dramatic and predictable. The major questions we are asking are "what is the effect of estrogens on the pattern of gene expression in target cells?", and "how does this pattern of gene expression produce growth and differentiation?". Estrogens can induce tumors in a variety of experimental systems and these hormones appear to be involved with human diseases such as breast, prostate, and endometrial cancers. Elucidation of the mechanisms of normal, physiological growth regulation by estrogens will in turn provide insights into control processes which may become deranged during hormonal carcinogenesis. At present we are studying the regulation of oncogene and growth factor receptor expression in the normal rodent uterus in response to estrogens, since overexpression of these normal cellular genes can cause transformation. In related studies, we are studying the patterns of expressions of these cellular oncogenes in animal models of estrogen-induced carcinogenesis to determine if they play a cause-effect role in tumor induction.
