Research Interests
Endocrinology, cancer chemotherapy
Our main interest is the study of hormones and their involvement in the causation of many of the most prevalent cancers. Particular emphasis is placed on studying the role of hormones, both natural and synthetic, and other growth regulators in the initiation, promotion, and progression of hormonal cancers, namely, breast, prostate, ovarian, and endometrium. Little is known about the complex cellular and molecular events leading to the induction of these hormonally-related neoplasms in either animals or humans.
Hormonal induction of neoplasia characteristically involves tissue and species specificity, sustained and prolonged hormonal exposure, and long induction or latency periods. Mechanisms of hormonal carcinogenesis involve enhanced cell proliferation and altered differentiation, protooncogene suppressor gene expression; and chromosomal alterations.
Our approach to elucidating mechanisms of hormonally-related cancer causation, particularly estrogens, is multi-disciplinary and includes: 1. molecular endocrinology: steroid-receptor interactions, metabolism of natural and synthetic hormones, hormonal regulation of DNA, RNA, and protein synthesis. 2. regulation of gene and protein expression, RNA synthesis and isolation, enzyme and protein synthesis, chromatin and chromosomal protein regulation. 3. cell and molecular biology: cell cycle (cyclins, cdks, inhibitors of p27, p21, p16) deregulation and cell proliferation; primary epithelial and tumor cell growth; growth factors; protooncogene expression (c-myc, c-jun, c-fos), gene amplification; suppressor gene expression (p53, WT1); genomic instability, karyotyping, molecular cytogenetics, CGH, and FISH.
The estrogen-induced ectopic uterine tumor in kidneys of the Syrian hamster and the estrogen-induced mammary tumor of the female ACI rat are the primary animal models used in these studies.
Li, J.J., and S.A. Li. Breast Cancer: Evidence for Xenoestrogen Involvement in Altering its Incidence and Risk. In: Natural and Anthropogenic Environmental Oestrogens: The Scientific Basis for Risk Assessment. J. Pure & Appl. Chem. 70:1713-1721 Li, S.A., D-Z Liao, J.J. Li. Estrogen-induced Breast Cancer in Female ACI Rats. In: Hormonal Carcinogenesis III (Eds. Li, J.J., J.R. Daling, S.A. Li), Springer-Verlag, New York, pp. 178-188, 2000.
Liao, D.J., X. Hou, S. Bai, S.A. Li, and J.J. Li. An Unusual Deregulation of Cell Cycle Components in Early and Frank Estrogen-induced Renal Neoplasias in the Syrian Hamster. Carcinogenesis, 21:2167-2173, 2000.
Li, J.J., S.J. Weroha, M.F. Davis, X. Hou, O. Tawfik, and S.A. Li. Estrogen and Progesterone Receptors in Renomedullary Interstitial Cells During Syrian Hamster Estrogen-induced Tumorigenesis: Evidence for Receptor-mediated Oncogenesis. Endocrinology, 142:4006-4014. 2001.
Li, J.J., and S.A. Li. Hormones and Carcinogenesis: Laboratory Studies. In: Principles and Practice of Endocrinology and Metabolism. (Ed. K.L. Becker), 3nd Edition, J.B. Lippinicott Co., New York, NY. Chap. 222, pp. 2024-2030, 2001.
Li, J.J., D. Papa, M.F. Davis, S.J. Weroha, M. Aldaz, K. El-Bayoumy, J. Ballenger, O. Tawfik, S.A. Li. Ploidy Differences Between Hormone- and Chemical Carcinogen-induced Mammary Neoplasms: Relation to Human Breast Cancer. Molec. Carcinogen., 33:56-65, 2002.
Mesia-Vela, S., R.I. Sanchez, J.J. Li, S.A. Li, A.H. Conney, and F.C. Kauffman. Catechol Estrogen Formation in Liver Microsomes from Female ACI and Sprague-Dawley Rats. Comparison of 2- and 4-hydroxylation. Carcinogenesis, 23:1369B1372, 2002.
Li, S.A., S.J. Weroha, O. Tawfik, and J.J. Li. Prevention of Solely Estrogen-induced Mammary Tumors by Tamoxifen: Evidence for Estrogen Receptor Mediation. J. Endocrinol., 175:297-305, 2002.
Jonathan J. Li, Ph.D.
Professor
Department of Pharmacology, Toxicology and Therapeutics
The University of Kansas Medical Center
MS1018
3901 Rainbow Boulevard
Kansas City, KS 66160
Phone: (913) 588-4760
Fax: (913) 588-4740
E-mail: jli1@kumc.edu
Curriculum Vitae in PDF Format
©
The University of Kansas Medical Center