New Radiation Oncology Researcher Joins Vanderbilt

March 19, 2010

BY: DAGNY STUART

David Gius, M.D., Ph.D., has joined Vanderbilt as associate professor of Radiation Oncology and Pediatrics.

Gius was associate program director of the National Institutes of Health (NIH) Oxford/Cambridge Scholars and the Trans-NIH MD/PhD Partnership Program, as well as chief of the National Cancer Institute’s (NCI) Molecular Radiation Oncology Section. He was also residency director of NCC Radiation Oncology Residency and clinical director of GYN services in the Center for Cancer Research and a researcher with the NCI in Bethesda, Md.

In addition to operating a research laboratory at Vanderbilt, Gius will see lung cancer patients in the Thoracic Oncology Clinic.

“I am pleased to join Vanderbilt’s robust program for basic and translational research into the mechanisms of diseases including human cancer,” said Gius.

David Gius, M.D., Ph.D.

Gius’ research is focused on the idea that tumor cells use pro-survival signaling pathways to evade the damaging effects of anti-cancer agents like chemotherapy drugs or ionizing radiation. He and his colleagues believe those signaling pathways are potential targets for drugs or other therapies to improve the cytotoxic effects of anti-cancer agents.

Research by Gius and his colleagues was featured in the Jan. 19, 2010 issue of Cancer Cell. Co-first authors Krish Patel, M.D., Center for Cancer Research, Hyun-Seok Kim, M.D., National Institute of Diabetes and Digestive and Kidney Diseases, and Gius focused on SIRT3, a member of the sirtuin family, which is localized in the mitochondria, the cellular compartment where energy is produced.

In collaboration with Sarki Abdulkadir, M.D., Ph.D., associate professor of Pathology at VUMC, they hypothesized that SIRT3 might function as a mitochondrial tumor suppressor protein.

Using a series of tissue culture, murine models and patient tissue samples, the researchers determined that SIRT3 is the first identified and characterized mitochondrial tumor suppressor protein. This work suggests that damaged and aberrant mitochondrial function, similar to gene mutations, may be an early event that ultimately leads to the development of cancers.

This idea was confirmed when the researchers found that mice genetically altered to delete SIRT3 developed estrogen and progesterone receptor (ER/PR) positive breast mammary tumors – a common characteristic of the kind of breast malignancies observed in older women. In tumor samples from women with breast cancer, SIRT3 expression was decreased, as compared to normal breast tissues.

Thus, the SIRT3 knockout model is one of only two mouse models established to scientifically investigate ER/PR positive breast tumor development.

Gius received his Bachelor of Science degree from the University of Illinois at Chicago and his medical degree from Loyola University of Chicago, Stritch School of Medicine. He earned his Ph.D. from the University of Chicago and completed post-doctoral fellowships at the University of Chicago, Department of Molecular Genetics and Cell Biology, and the Department of Radiation and Cellular Oncology.

Prior to joining the NCI, he served as assistant professor and residency director, Radiation Oncology Center, Washington University School of Medicine, St. Louis.

In addition to research, Gius is committed to developing the next generation of investigators. “I consider education and service as a key aspect of my laboratory and clinical work,” Gius explained.

Gius has published more than 70 peer reviewed manuscripts in journals such as Nature, Cancer Cell, PNAS, Molecular and Cellular Biology, and Cancer Research. He is an associate editor for Cancer Research and a permanent member of the NIH Radiation and Therapeutics and Biology Study Section.

No Comments

No comments yet.

Sorry, the comment form is closed at this time.