Director, Molecular & Cellular Biology Graduate Program Co-director, Radiation and Antioxidant Enzyme Core Service Co-director, Free Radical Cancer Biology Program Professor of Radiation Oncology Professor of Pathology, Surgery
Primary Office: B180 ML
Iowa City, IA 52242


BS, Chemistry, University of Wisconsin, Platteville, Wisconsin
PhD, Human Cancer Biology, University of Wisconsin, Madision, Wisconsin

Post Doctorate, Department of Radiation Oncology, Arizona Cancer Center, The University of Arizona
Post Doctorate, Department of Pharmacology & Toxicology, , The University of Arizona, Arizona Cancer Center

Education/Training Program Affiliations

Department of Pathology Graduate Program
Free Radical and Radiation Biology Graduate Program
Interdisciplinary Graduate Program in Human Toxicology
Interdisciplinary Graduate Program in Molecular and Cellular Biology
Interdisciplinary Graduate Program in Translational Biomedicine
Medical Scientist Training Program

Research Summary

My laboratory focuses on the transcriptional regulation of cancer related genes including oncogenes and tumor suppressor genes. Specifically, we are studying the molecular mechanisms by which aberrant cytosine methylation of CpG dinucleotides affects gene expression during the development of cancer. We have focused primarily on the tumor suppressor gene SOD2 that encodes the antioxidant enzyme superoxide dismutase. We have determined that site specific DNA methylation of the SOD2 gene promoter can suppress its transcriptional activation. Thus, cytosine methylation of genetic regulatory elements within this important tumor suppressor gene can mediate its inactivation. We are also studying transcription factor AP-2 and its interactions with the SOD2 promoter. Interestingly, these interactions are affected by DNA methylation. We are also assessing chromatin accessibility in the region of the SOD2 promoter in cells that differentially express the gene. Our future research directions will be aimed at elucidating the role of cytosine methylation as a mechanism for inactivation of other genes involved in protection against oxidative damage as well as other classical tumor suppressor genes, and to elucidate the mechanism(s) by which CpG methylation can bring about these changes in gene expression. We have recently become interested in cancer therapy using the human sodium iodide symporter. When expression of this gene is activated, either by gene transfer of epigenetic reactivation, tumor cells acquire the thyroid-like phenotype of iodide concentration. This activity can be exploited as a tool for imaging gene delivery and expression in humans in clinical translational trials of gene therapy; or as a means to deliver therapy itself depnding on which radioisotope of iodine is used.

Center, Program and Institute Affiliations

Cancer and Aging Program
Center for Gene Therapy of Cystic Fibrosis and other Genetic Diseases
Environmental Health Sciences Research Center
Fraternal Order of Eagles Diabetes Research Center
Holden Comprehensive Cancer Center
Institute for Clinical and Translational Science
Iowa Initiative in Human Genetics

Selected Publications

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Nelson M, Domann F, Bowden G, Hooser S, Fernando Q, Carter D.  Effects of acute and sub-chronic exposure of topically applied fullerene extracts on the mouse skin.  Toxicol. Ind. Health.  1993. 9(4):623-630. 

Clifton K, Domann F, Groch K.  On the cells of origin of radiogenic thyroid cancer: New studies based on an old idea..  J. Radiat. Res.  1991. 32:143-155. 

Domann F, Mitchen J, Clifton K.  Restoration of thyroid function following total thyroidectomy and quantitative thyroid cell transplantation.  Endocrinology.  1990. 127(6):2673-2678. 

Seed T, Kaspar L, Domann F, Niiro G, LeBuis D.  Developmental and radiobiologic characteristics of canine multinucleated, osteoclast-like cells generated in vitro from canine bone marrow.  Scanning Microsc.  1988. 2(3):1599-1611. 

Watanabe H, Tanner M, Domann F, Gould M, Clifton K.  Inhibition of carcinoma formation and of vascular invasion in grafts of radiation-initiated thyroid clonogens by unirradiated thyroid cells.  Carcinogenesis.  1988. 9(8):1329-1335.