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Present Position
Professor and Vice Chair, Department of Pathology and Laboratory Medicine Director of the Viral and Chemical Carcinogenesis Program Area, UCLA, Jonsson Cancer
Comprehensive Cancer Center
Director, Molecular Toxicology Interdepartmental Doctoral Program Member, UCLA Molecular Biology Institute
Education
1967 B.Sc. (Genetics) Edinburgh University, Scotland. 1972 Ph.D. (Genetics) Cambridge University, England.
Postdoctoral Training
1972-’74 Genetics Unit, Massachusetts General Hospital and Harvard Medical School. 1974-’75 Eleanor Roosevelt Institute for Cancer Research, University of Colorado Medical Center 1975-’79 Department of Molecular Biology, University of California, Berkeley.
Research Interests
Dr. Hankinson’s research focuses on the mechanism of carcinogenesis by polycyclic aromatic hydrocarbons (found in cigarette smoke and smog) and dioxin (a widespread pollutant), and related compounds. Carcinogenesis by these compounds depends upon their binding to the aryl hydrocarbon receptor (AHR) and the subsequent dimerization of AHR with the ARNT protein. He is studying the molecular mechanism of activation of gene transcription by the liganded AHR/ARNT dimer (including the role of coactivator proteins in this process) and is analyzing a number of novel dioxin-inducible genes his group has discovered. In addition, he also studies the roles of AHR and ARNT in animal models of carcinogenesis. ARNT also dimerizes with HIF-1a to form HIF-1 (Hypoxia Inducible Factor), which is the master regulator of the hypoxic response. Dr. Hankinson is studying the molecular mechanism of gene activation by HIF-1 and the role of HIF-1 in tumor angiogenesis and growth.
The current research in his laboratory focuses on the following :
- Analyzing the mechanism of transcriptional activation by the AHR/ARNT and HIF-1a/ARNT dimers, particularly the potential roles of coactivator proteins in theses processes.
- Isolating additional genes that are transcriptionally activated by the AHR/ARNT dimer and that may therefore be involved in chemical carcinogenesis.
- Isolating and analyzing genes transcriptionally activated by hypoxia.
- Determining the role of ARNT in development, response to hypoxia, and response to chemical carcinogens, via analysis of ARNT "conditional knockout" mice.
Recent Publications
Roth, M.D., Marquez-Magallanes, J.A., Yuan, M., Sun, W., Tashkin, D.P., Hankinson, O. (2001). Induction and Regulation of the Carcinogen-Metabolizing Enzyme, CYP1A1, by Marijuana Smoke and Delta(9)-Tetrahydrocannabinol. Am. J. Respir. Cell. Mol. Biol. 24: 339-344.
Lei, X.-D., Chapman, B., Hankinson, O. (2001). Loss of CYP1A1 Messenger RNA Expression Due to Nonsense-Mediated Decay. Mol. Pharmacol. 60: 388-393.
Anttila, S.L., Tuominen, P., Hirvonen, A., Karjalainen, A., Hankinson, O., Elovaara, E. (2001). CYP1A1 levels in lung tissue of tobacco smokers and polymorphisms of CYP1A1 and aromatic hydrocarbon receptor. Pharmacogenetics. 11: 501-509.
Yoon, D.Y., Buchler, P., Saarikoski, S.T., Rivera, S.P., Hines, O.J., Reber, H.A., Hankinson, O. (2001). Identification of genes differentially induced by hypoxia in pancreatic cancer cells. Biochem. & Biophys. Res. Comm. 288: 882-886.
Rivera, S.P., Saarikoski, S.T., Hankinson, O. (2002). Identification of a novel dioxin-inducible cytochrome P450. Mol. Pharm. 61: 255-259.
Wang, S., and Hankinson, O. (2002). Functional involvement of the BRM/SWI2-related gene 1 protein (BRG-1) in cytochrome P4501A1 transcription mediated by the aryl hydrocarbon receptor complex. J. Biol. Chem. 277: 11821-11827.
Beischlag, T.V., Wang, S., Torchia, J., Reisz-Porszasz, S., Muhammad, K., Nelson, W.E., Probst, M.R., Rosenfeld, M.G., Hankinson, O. (2002). Recruitment of the NCoA/SRC-1/p160 Family of Transcriptional Co-activators by the Aryl Hydrocarbon Receptor/Aryl Hydrocarbon Receptor Nuclear Translocator Complex. Mol. Cell. Biol. 22: 4319-4333.
Saarikoski, S.T., Rivera, S.P., Hankinson, O. (2002). Mitogen-inducible gene-6 (mig-6), adipophilin and tuftelin are inducible by hypoxia. FEBS Lett. 530: 186-90.
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