Rebecca Oberley-Deegan

Associate Professor, Biochemistry and Molecular Biology 

Deegan2020.pngPhone: 402-559-9364 (Office)
    Location: BCC 6.12.391
Fax: 402-559-6650
B.A. Grinnell College, Grinnell, Iowa - 1999
Ph.D. University of Iowa, Iowa City Iowa - 2004
Postdoctoral training at National Jewish Health, Denver, CO

Research Opportunities in my laboratory:
Not currently accepting new graduate students and or MD/PhD students


The focus of Dr. Oberley-Deegan’s laboratory is to reduce side effects associated with cancer therapy. Our main goal is to reduce radiation and chemotherapy induced toxicity to normal tissues while not protecting the tumor cells from being killed by these therapies. We have 4 main areas of focus in our laboratory: 1. Protection of normal tissues undergoing radiation therapy, 2. Protection of normal tissues exposed to chemotherapy, 3. Determine the role of tumor progression when mitigating normal tissue toxicity, 4. Clinical trials in Head and Neck and Anal Cancer using a promising new radioprotector.

  1. Radiation toxicity: Fibrosis and cancer have been described as unsuccessful attempts at wound healing. Both processes begin with the de-differentiation of normal cells, resulting in uncontrolled proliferation and remodeling of the extracellular matrix. Reactive oxygen species (ROS) are thought to be one of the main drivers for both fibrosis and cancer progression. Elevated ROS, through radiation exposure, promotes epigenetic modifications of prostate cancer cells leading to a more aggressive tumor. Radiation also epigenetically modifies normal fibroblasts into myofibroblasts, which results in aberrant extracellular matrix deposition and ultimately causing fibrosis. Dr. Oberley-Deegan’s laboratory is focused on understanding the mechanisms by which ROS promote radiation induced fibrosis and prostate cancer progression.  Her research has shown that scavenging radiation-induced ROS, through the addition of a novel catalytically active antioxidant, results in the protection of fibrosis of normal tissues following radiation and enhanced sensitivity of prostate tumors to radiation.
  2. Chemotherapy toxicity: Chemotherapy can result in severe toxicity to normal cells during treatment for cancer, such as bone marrow suppression and cachexia. This toxicity can be so severe that therapy has to halt for these patients and currently there are no treatment for these side-effects. ROS is a major driver of these chemotherapy-induced toxicities, which result in cell death and tissue atrophy. Dr. Oberley-Deegan’s laboratory has demonstrated that reduction of ROS leads to reduction of chemotherapy-induced toxicity of normal tissues. Currently, her lab is further elucidating the mechanisms by which ROS causes toxicity through chemotherapy use in cancer patients.
  3. Tumor progression: In order to protect from radiation or chemotherapy toxicity, the tumor tissue still needs to be selectively killed. The Oberley-Deegan is currently working with in vitro and in vivo models of prostate, colorectal and pancreatic cancer to further understand the role of ROS in the progression of cancer growth and cancer killing in combination with radiation or chemotherapy.
  4. Dr. Oberley-Deegan’s laboratory is involved in two clinical trials currently ongoing at UNMC. There is a Phase I trial to investigate the role of a catalytic antioxidant as a radioprotector for anal cancer patients. There is a Phase II trial with these same compound in head and neck cancer patients.



My Publications

Current grants:

NIH 1 RO1 CA178888: “MnTE-2-PyP as a radioprotector in prostate cancer therapy”