Victoria Perepelitsa

Dr. Belancio was born in Berlin, Germany. She obtained her BS and MS degrees in Cytology and Genetics from Novosibirsk State University in Novosibirsk, Russia. She studied Medical Genetics at the University of Alabama at Birmingham. She received her doctoral degree in Molecular and Cellular biology from the Department of Epidemiology at Tulane University in New Orleans. She did her postdoctoral training with Dr. Prescott Deininger at Tulane University. She has been a faculty member in the Department of Structural and Cellular Biology, Tulane School of Medicine since 2008 and is a member of the Tulane Center for Aging. Dr. Belancio’s primary research interests are focused on genetic instability and cellular responses associated with the activity of mammalian retroelements. She is studying molecular mechanisms controlling the expression of and the damage from these elements in normal and cancer cells. Dr. Belancio is a member of the Tulane Center for Aging. 

Dr. Victoria P. Belancio, Associate Professor of Structural and Cellular Biology at Tulane School of Medicine, is broadly recognized for her original contributions to understanding the impact of retrotransposons on genome stability and disease. Her first major discovery involved identification of novel mechanisms attenuating expression and damage caused by LINE-1 retrotransposons. She was a key contributor to the establishment of somatic expression of LINE-1 in many normal human tissues, a finding that has triggered a broad recognition of somatic LINE-1 damage and its relevance to human disease and aging. Through her ongoing interest in understanding regulation of LINE-1 expression and activity in vivo, Dr. Belancio discovered an important connection between LINE-1 retrotransposons and melatonin signaling, a major component of the host circadian system. Using a unique tissue-isolated model of human cancer, her lab identified that nocturnal melatonin suppresses LINE-1 expression and retrotransposition through the activation of the G-protein coupled receptor melatonin receptor 1 (MT1). This unforeseen in vivo relationship between LINE-1-induced damage and melatonin signaling strongly supports that experiencing light exposure at night, which disrupts nocturnal melatonin production, may upregulate LINE-1 activity. Thus, shift workers and urban residents, who are continually subjected to artificial light at night, as well as the elderly, who experience age-dependent loss of nocturnal melatonin production, may have a higher risk of cancer due to the increase in genomic instability associated with LINE-1 damage. This finding was recognized by the U. S. National Academy of Science and the Alexander von Humboldt Foundation 18th annual German-American Kavli Frontiers of Science symposium in Potsdam, Germany.