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Kelly Jean Thomas, PhD

Postdoctoral Fellow

Kelly Jean Thomas received her Bachelor in Science in 2004 from the University of Kansas studying genetics. During this time, she received multiple undergraduate research training grants to study immunological disorders including Wiskott-Aldrich syndrome at Washington University School of Medicine, systemic lupus erythematosus at the University of Kansas and human immunodeficiency virus at University of Capetown in South Africa.

She accepted a post-baccalaureate research position in 2004 at the molecular genetics unit at the National Institute on Alcohol Abuse and Alcoholism at the National Institutes of Health to study the genetic susceptibility of addiction.

She received her PhD in biochemistry and molecular biology from Georgetown University School of Medicine in 2009. Her dissertation work was completed in the gene expression unit at the National Institute on Aging at the National Institutes of Health; she investigated the role of mitochondrial dysfunction in the development of neurological disorders, in particular, Parkinson disease.

She began her postdoctoral fellowship at St. Mary's Saccomanno Research Institute in 2009. She also serves as an adjunct faculty member in the biology department of Mesa State College.

Research Interests
Dr. Thomas investigates the role of mitochondrial dysfunction in the etiology of cancer. Mitochondria not only provide energy for cells, but they participate in numerous metabolic reactions, such as providing antioxidant defenses, and play a central role in normal programmed cell death (apoptosis)-a tightly regulated process which is overridden during the transformation process.

Mitochondrial dysfunction and mutations in mitochondrial DNA have been reported in cancer cells, partly due to the damaging effects of ROS. Mitochondrial profiling experiments have identified unique signatures from transformed cells; however, the phenotypes from these genetic alterations have yet to be identified. The Warburg effect demonstrates that tumor formation is accompanied by a dysregulation of energy production and metabolism. A better understanding of cancer metabolism with respect to the role of mitochondria in tumor progression is needed. Future studies will evaluate mitochondrial function in normal and lung cancer cell lines and their stem-cell like subpopulations, comparing the metabolic output amongst cells having varying degrees of tumorigenicity. Changes in mitochondrial function will be identified to determine if a relationship exists between tumor progression and mitochondrial dysfunction.

Click PubMed.gov for a listing of publications by Kelly Jean Thomas.

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