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.
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Pending patents:
U.S. Patent application 60/445,945 (filed on February 7, 2003).
Deininger, Prescott L. and Victoria Perepelitsa Belancio
Entitled:Mammalian Retrotransposable Elements
U. S. Patent application 14/943,942 (filed on November 14, 2015, approved 2019).
Sokolowski Mark and Belancio Victoria P.
Entitled: ANTIBODIES THAT INHIBIT LONG INTERSPERSED ELEMENT-1 RETROTRANSPOSON ENDONUCLEASE
Current and former trainees:
2019-present - Qianhui Du, Tulane BMS graduate student
2017-present - Ben Freeman, Tulane BMS graduate student
2015-2017 - May Chynces, Graduate student Multidisciplinary Program in Aging
2014-2017 - Madison Smither, Ben Franklin High School intern (Jefferson Scholar, The University of Virginia)
2012-2017 - Dr. Mark Sokolowski, Tulane BMS graduate student (postdoc at Masonic Cancer Center, University of Minnesota, Minneapolis, MN)
2013-2016 - Dr. Claiborne M. Christian, Tulane BMS graduate student (postdoc at St. Jude Children's Research Hospital, Memphis, TN)
2009- 2016 - Dr. Kristine Kines, postdoc (scientist at the Centers for Disease Control and Prevention, Atlanta, GA)
2013-2014 - James Flotken, Tulane undergraduate student intern (Tulane School of Medicine)
2011-2012 - Lakshya Bajaj, Hayward Human Genetics master student (graduate student at Baylor College of Medicine Graduate School of Biomedical Sciences)
2009-2010 - Angela Liu, Environmental Health Science master student (Ph.D. program in epidemiology at the University of North Carolina at Chapel Hill)
Member:
COMET (Consortium of Transposable Elements at Tulane)
Tulane Cancer Center
Tulane Circadian Cancer Biology Group
Tulane Center for Aging
Tulane Cancer Center Program Member
Only a small proportion of the human genome actually codes for proteins, begging the question of what the rest of our genetic material actually does. Human retrotransposons, long dismissed as inert repetitive sequences of "junk DNA," are quite active and can profoundly influence our genomes. Our lab studies one type of these sequences, termed Long Interspersed Element 1 (LINE1 or L1 for short). Through the use of its two proteins encoded in its bicistronic mRNA (ORF1p and ORF2p), L1 is able to copy and paste itself into new genomic locations. L1 proteins (particularly ORF2p, which contains two enzymatic functions endonuclease and reverse transcriptase) are also used by other parasitic elements (SINEs, Short Interspersed Elements, and SVA) to move about the genome. Furthermore, L1 machinery is responsible for the generation of processed pseudogenes. L1 is thus the direct and indirect progenitor of a sizable chunk of our genome. Until recently, retrotransposition was believed to take place predominantly in the germ line. The current view is that L1 expression and retrotransposition also occurs in somatic cells, with tumors being particularly permissive for L1 activity.
Retrotransposition is only one of (albeit the best studied) ways L1 can damage our genome. L1 ORF2p, through its endonuclease, can induce DNA double strand breaks that can introduce a spectrum of mutations if not repaired faithfully, trigger cellular senescence, or even lead to apoptotic cell death.
L1, SINE, and SVA sequences can influence gene function and genome organization long after integration by bringing along their functional promoters, polyadenylation signals, and splice sites; usage of which can alter gene expression or generate novel chimeric transcripts. Additionally, all repetitive sequences can undergo homologous recombination, leading to deletion or duplication of genetic material which can at times be mutagenic. Over the course of evolution, the human genome accumulated a staggering 500,000 copies of L1 and over 1,000,000 copies of the human SINE Alu. Fortunately for our cells, most of these loci are inactive. However, non-allelic homologous recombination between these highly-related sequences still causes a wide spectrum of human diseases.
Despite its ubiquity and evolutionary influence, many details of L1 replication cycle, as well as the basic functions and interaction profiles of the L1 proteins remain unknown. Our lab is working to elucidate some of these unknowns from a number of angles and fronts. Our research interests are focused on the contribution of L1 to human disease (particularly cancer and other age-associated diseases) and include:
the RNA and protein biology of L1 as well as the influence of the circadian system (how cells in a complex organism tell time) on L1 activity
characterization of the cytotoxic properties of the ORF2p endonuclease domain and cellular response to L1 activity
characterization of L1 protein expression and regulation in the mammalian environment
Our lab is unique in that we employ a wide array of basic science strategies to study the L1 replication cycle, from basic molecular biology all the way unto animal models. We routinely perform DNA, RNA,and protein analyses, in addition to tissue culture-based experiments and Next Generation Sequencing approaches.
My lab is a part of the Tulane Cancer Center, Tulane Circadian Cancer Biology group, and COMET, the Consortium of Transposable Elements at Tulane. If you would like more specifics on any of our many projects, please do not hesitate to contact me.
Click Here For PubMed Publications
Click here to access complete list of NCBI publications.
Books:
Chronobiology and rhythms in relation to health, ageing and longevity. Edited by Belancio VP., Hill SM, and Jazwinski SM. Volume V in Healthy Ageing and Longevity series, Springer, series editor Rattan S. (2017)
Selected Invited Talks:
Tulane Cancer Center Program Member
Only a small proportion of the human genome actually codes for proteins, begging the question of what the rest of our genetic material actually does. Human retrotransposons, long dismissed as inert repetitive sequences of "junk DNA," are quite active and can profoundly influence our genomes. Our lab studies one type of these sequences, termed Long Interspersed Element 1 (LINE1 or L1 for short). Through the use of its two proteins encoded in its bicistronic mRNA (ORF1p and ORF2p), L1 is able to copy and paste itself into new genomic locations. L1 proteins (particularly ORF2p, which contains two enzymatic functions endonuclease and reverse transcriptase) are also used by other parasitic elements (SINEs, Short Interspersed Elements, and SVA) to move about the genome. Furthermore, L1 machinery is responsible for the generation of processed pseudogenes. L1 is thus the direct and indirect progenitor of a sizable chunk of our genome. Until recently, retrotransposition was believed to take place predominantly in the germ line. The current view is that L1 expression and retrotransposition also occurs in somatic cells, with tumors being particularly permissive for L1 activity.
Retrotransposition is only one of (albeit the best studied) ways L1 can damage our genome. L1 ORF2p, through its endonuclease, can induce DNA double strand breaks that can introduce a spectrum of mutations if not repaired faithfully, trigger cellular senescence, or even lead to apoptotic cell death.
L1, SINE, and SVA sequences can influence gene function and genome organization long after integration by bringing along their functional promoters, polyadenylation signals, and splice sites; usage of which can alter gene expression or generate novel chimeric transcripts. Additionally, all repetitive sequences can undergo homologous recombination, leading to deletion or duplication of genetic material which can at times be mutagenic. Over the course of evolution, the human genome accumulated a staggering 500,000 copies of L1 and over 1,000,000 copies of the human SINE Alu. Fortunately for our cells, most of these loci are inactive. However, non-allelic homologous recombination between these highly-related sequences still causes a wide spectrum of human diseases.
Despite its ubiquity and evolutionary influence, many details of L1 replication cycle, as well as the basic functions and interaction profiles of the L1 proteins remain unknown. Our lab is working to elucidate some of these unknowns from a number of angles and fronts. Our research interests are focused on the contribution of L1 to human disease (particularly cancer and other age-associated diseases) and include:
the RNA and protein biology of L1 as well as the influence of the circadian system (how cells in a complex organism tell time) on L1 activity
characterization of the cytotoxic properties of the ORF2p endonuclease domain and cellular response to L1 activity
characterization of L1 protein expression and regulation in the mammalian environment
Our lab is unique in that we employ a wide array of basic science strategies to study the L1 replication cycle, from basic molecular biology all the way unto animal models. We routinely perform DNA, RNA,and protein analyses, in addition to tissue culture-based experiments and Next Generation Sequencing approaches.
My lab is a part of the Tulane Cancer Center, Tulane Circadian Cancer Biology group, and COMET, the Consortium of Transposable Elements at Tulane. If you would like more specifics on any of our many projects, please do not hesitate to contact me.
2010-present - Director of the Tulane Cancer Center seminar Series
2010 - Louisiana Cancer Research Consortium Award for Outstanding Scientific Achievement in the Genetics program,
2012 - Kavli fellow, the U. S. National Academy of Scienceand Alexander von Humboldt Foundation 18th annual German-American Kavli Frontiers of Science symposium,Potsdam, Germany (by invitation only)
2015 - NCI-sponsored work-shop "The Role of Mobilome in Cancer" to identify and evaluate emerging research areas with high potential for advancing our understanding of cancer processes and contributing to the NCI research portfolio, NCI Shady Grove campus, Rockville, MD(by invitation only)
2015 - James de la Houssaye Mentor Award Greater New Orleans Science and Engineering Fair
2016-present - Emmy Noether Student to Scientist Award selection committee
2019 - co-organizer of the FASEB Mobile elements and Genomes conference: https://src.faseb.org/mobile-dna/Home
Grant review:
NIH, NSF, Fondazione Telethon
Current Funding:
NIH/NIA, NIH/NIEHS, Brown Foundation, Brown Foundation Emmy Noether Program
Past Funding:
DOD, NIH, The Ellison Medical Foundation, Kay Yow Cancer Fund/V Foundation, Life Extension Foundation, BORSF, Ladies Leukemia League, Edward G. Schlieder Foundation
