Cast Your Vote: Select the New EMGS Officers for 2019-2020
The EMGS Nominating Committee has selected the candidates for this year’s election. This year we will be choosing a Vice President-Elect, a Treasurer, and five Councilors. Each candidate has agreed to volunteer their time and energy to serve both the Society and its members.
The ballot will close on December 27, 2019.
Vice President-Elect Candidates
Dr. Ben Van Houten
University of Pittsburgh
Dr. Bennett Van Houten is the Richard M. Cyert Professor of Molecular Oncology, in the Department of Pharmacology and Chemical Biology, and a member of the Molecular Biophysics & Structural Biology Graduate faculty. Dr. Van Houten is the co-leader of the Genome Stability Program at the UPMC-Hillman Cancer Center, where he oversees a group of scientists studying genome stability and cancer. He is also the Associate Director for Basic Research in the UPMC and University of Pittsburgh Aging Institute.
Dr. Van Houten received his Bachelor’s degree from Clarion University and his Ph.D. from the University of Tennessee at the Oak Ridge Graduate School of Biomedical Sciences, in Oak Ridge, Tennessee in 1984. Ben did his postdoctoral training with Professor Aziz Sancar who was recognized with a Nobel Prize for Chemistry in 2015 for his mechanistic insights into DNA repair. Prior to moving to the University of Pittsburgh, Dr. Van Houten was the Chief of the Program Analysis Branch in the Division of Extramural Research and Training and Senior Investigator in the Laboratory of Molecular Genetics in the Division of Intramural Research at National Institute of Environmental Health Sciences, NIH from 1999-2008. While at the NIEHS, Dr. Van Houten helped develop a publication tracking system, Scientific Publication Information Retrieval and Evaluation System (SPIRES), which is now used by all of NIH in RePORTER. He was recognized with five NIH Merit Awards, and a NIH Director’s Award, and for his service to science was awarded a Medal of Science by the Slovak Academy of Sciences in 2008.
Dr. Van Houten’s laboratory is doing cutting-edge research in two major areas, namely the structure and function of DNA repair enzymes at the single molecule level, and the role of mitochondria in cancer and neurodegenerative diseases. Dr. Van Houten’s laboratory is currently supported by three NIEHS funded grants (PI), and is a co-investigator on two other NIH grants.
- 2R01ES019566-09 & 1R01ES028686-02, which use state-of-the-art single molecule approaches, including atomic force microscopy and oblique angle fluorescence to watch quantum-dot labeled DNA repair molecules interrogate DNA for structural alternations in real time. The long term goal of this project is to watch multiple protein machines do work on DNA at the single molecule level in purified systems, nuclear cell extracts and in living cells.
- R33ES025606-04, a collaboration with Drs. Patty Opresko, Simon Watkins, Marcel Bruchez and Ed Burton and seeks to understand how singlet oxygen damage targeted to either the mitochondria or telomeres can have reciprocal effects on each other. This approach is being used to examine the fate of 8-oxoG lesions at telomeres and the role of ROS damage in a zebrafish model of Parkinson’s disease.
Dr. Van Houten has trained 43 postdoctoral fellows and graduate students. He holds four patents (two additional applications are pending), and has authored over 235 scientific articles, co-edited a book on DNA damage recognition, a volume of single-molecule techniques in DNA repair, and has also published 28 book chapters and reviews. He has chaired Gordon Conferences on Genetic Toxicology and Oxidative Stress and disease. He has served as Chair of the Cancer Etiology study section. His Web of Science, h-index is 68. Dr. Van Houten currently serves as an Associate Editor for DNA Repair, and serves on the editorial board of Molecular Carcinogenesis.
Dr. Joann B. Sweasy
University of Arizona Cancer Center
Joann B. Sweasy earned her doctoral degree from Rutgers University, studying the role of the RecA protein in the SOS response to DNA damage, under the direction of Dr. Evelyn M. Witkin.
She initiated her research on the fidelity of DNA synthesis at the University of Washington in Dr. Lawrence Loeb’s laboratory. After joining Yale University School of Medicine in 1993, she rose through the ranks to become the Ensign Professor of Therapeutic Radiology and Associate Director for Basic Sciences at the Yale Cancer Center. She is currently a tenured professor in Cellular and Molecular Medicine and is Associate Director, Basic Sciences at the University of Arizona Cancer Center.
Dr. Sweasy is an internationally recognized expert in the genetics, cell biology, and biochemistry of DNA repair. For the past 25 years, her laboratory has been consistently funded by the National Cancer Institute to study the molecular basis of mutagenesis and dysfunctional DNA repair as they relate to human diseases including cancer and autoimmunity.
Dr. Sweasy’s research team recently discovered that dynamic conformational changes are important for accurate DNA synthesis. The team has also shown that human germline and somatic genetic variants of base excision repair genes are linked to carcinogenesis because they are unable to properly remove damaged DNA bases, leading to genomic instability, mitotic catastrophe, and other cancer-associated phenotypes. The Sweasy laboratory also discovered that aberrant DNA repair leads to the development of lupus. Her current focus in this area is the identification and characterization of germline DNA repair variants that are enriched in individuals with lupus.
Dr. Sweasy has served on the EMGS Council, as a Member of the Executive Committee, Co-leader of the DNA Repair SIG, and is currently the Chair of the Program Committee for the 2020 EMGS meeting. Dr. Sweasy has significant skills in and commitment to training the next generation of biomedical scientists. Dr. Sweasy is especially proud of being presented with the 2017 Yale Postdoctoral Mentoring Award. Over 50% of her trainees are women and include several individuals from diverse backgrounds. Several of Dr. Sweasy’s projects are collaborative in nature and as the lead P.I., she has successfully directed the studies, ensuring scientific rigor and the use of unbiased methodology, resulting in the publication of several high-quality papers in peer-reviewed journals.
Dr. Christi A. Walter
UT Health Science Center at San Antonio
Dr. Chris Walter received a Ph.D. from Florida State University, then completed a postdoctoral fellowship at UT MD Anderson Cancer Center. She completed a second postdoctoral fellowship in human cytogenetics and molecular genetics at UT Health San Antonio and became a diplomate of the American Board of Medical Genetics.
Dr. Walter started as an Assistant Professor in the Department of Cellular & Structural Biology (now Cell Systems & Anatomy), Associate Director of the Clinical Cytogenetics Laboratory, and Director of the Transgenic Rodent facility. After receiving tenure and moving through the academic ranks, she became Interim Chair then Chair of the Department of Cell Systems & Anatomy, a position she continues today. She served as chair of the NIA B study section and was a member of the Gerontological Society of American Public Policy Committee. Related activities include service on the Science Advisory Board Chemical Assessment Committee for the EPA, membership on the local host committee for the World Stem Cell Summit 2014, and other professional activities.
Dr. Walter’s research program is multidisciplinary, combining cell and reproductive biology, DNA repair, mutagenesis and aging. Her laboratory is focused largely on base excision repair and mutagenesis in biological processes such as germ cell aging and hepatocellular carcinoma. Her laboratory discovered that AP endonuclease (APE1) is a critical factor in these processes using mouse models. Her lab provided molecular insights into a mechanism that drives the increase in mutations in male germ cells with reproductive aging, a phenomenon known as the paternal age effect. The paternal age effect is associated with diseases such as autism spectrum disorders and several autosomal dominant diseases. Using a mouse model of spontaneous hepatocellular carcinoma, her lab showed that 06-methylguanine-DNA methyltransferase and base excision repair may be important in the etiology and/or treatment of this cancer.
Dr. Melike Caglayan
UF Health Cancer Center
Dr. Caglayan completed her postdoctoral research at the National Institutes of Health (NIH), National Institute of Environmental Health Science (NIEHS) in the DNA Repair Group headed by Dr. Samuel H. Wilson. During that time, she studied the molecular mechanisms of base excision repair (BER) by characterizing protein-protein interactions and their role in coordinating the sequential enzymatic steps of the BER pathway using biochemistry and cell biology approaches.
During her postdoctoral fellowship, Dr. Caglayan was highly successful and became established as an outstanding young investigator. She completed five first author reports including three first author in the outstanding journals [Caglayan M. et. al., Nat. Struc. and Mol. Biol., 2014; Caglayan M. et. al., Nat. Comm., 2017; Caglayan M. et. al., Nat. Comm., 2018], and two reviews as first author and she also contributed to four collaborative publications. Among a variety of accomplishments, she developed an independent research project in the mammalian base excision repair field and was awarded the NIH Pathway to Independence Award (K99/R00) grant entitled “Oxidant and environmental toxicant-induced effects compromise ligation in DNA repair” from NIEHS.
She recently transitioned to an independent faculty position at the Department of Biochemistry and Molecular BioIogy, University of Florida as a tenure-track Assistant Professor. There she is continuing her work on this topic [Caglayan M. J. Mol. Biol. 2019], funded by University of Florida Health Cancer Center Startup Fund. Dr. Caglayan’s laboratory has been studying the DNA damage processing of cytotoxic and mutagenic lesions that arise from environmental agents. Her laboratory focuses on the molecular mechanism of BER pathway that protects cells from the effects of endogenous stressors and environmental toxicants to better understand the importance and mechanism of the sequential flow of DNA intermediates into repair pathway control and modulation enabling genome stability in humans as a function of environmental toxicant-induced cytotoxicity.
Dr. Elise Fouquerel,
Thomas Jefferson University and SKMC
Dr. Fouquerel is an Assistant Professor in the department of Biochemistry and Molecular Biology at Thomas Jefferson University and Sydney Kimmel Medical College since December 2018.
She completed her Ph.D. at the University of Strasbourg in France where she studied the role of PARP enzymes in DNA repair and replication. She pursued a Postdoctoral training at the University of Pittsburgh with Dr. Robert W. Sobol studying the impact of alkylatin DNA damage-mediated PARP1 hyperactivation on cell metabolism. She then joined Dr. Patricia Opresko lab where she focused on deciphering the mechanisms driving telomere dysfunction upon oxidative stress.
In 2016, she received funding from NIEHS in form of K99/R00 Pathway to Independence Award which paved the way for her current research addressing the roles of PARP enzymes in the preservation of telomere integrity upon genotoxic exposures. PARP1 enzyme has emerged as a highly relevant drug target in cancer patients. Dr. Fouquerel’s contributes to inform the rational design of PARP1-directed therapeutic strategies and help in the design of new approaches for cancer treatment and aging-related diseases.
Dr. Michael G. Kemp
Wright State University
Dr. Michael Kemp is an Assistant Professor in the Department of Pharmacology and Toxicology at the Wright State University Boonshoft School of Medicine in Dayton, Ohio. He received both a B.S. in Biological Sciences (1999) and Ph.D. in Biomedical Sciences (2006) from Wright State University, where he developed his initial interest in DNA metabolism. Dr. Kemp then moved to the University of North Carolina to train with Nobel Laureate Aziz Sancar M.D., Ph.D. and was involved in several projects associated with the mechanisms of nucleotide excision repair and DNA damage checkpoint signaling and their regulation by the circadian clock. After nearly a decade in the Sancar laboratory as a postdoctoral researcher and then as a research faculty member, Dr. Kemp returned to Wright State University in 2016 to receive additional training in skin biology and to begin to translate his basic research interests to human skin.
Dr. Kemp’s laboratory at Wright State University is focused on understanding how human cells and human skin responds to DNA damage induced by both environmental carcinogens and pharmaceutical compounds. This work involves both fundamental studies of DNA repair and DNA damage kinase signaling in vitro and translational work with skin biopsies from human subjects both ex vivo and in vivo. In addition to developing new assays and read-outs of the DNA damage response in human skin, one of the goals of the Kemp laboratory is to understand why geriatric skin is at greater risk of developing non-melanoma skin cancers than the skin of younger individuals.
Dr. Kemp has been a member of the EMGS since 2016 and is currently a member of the Awards and Honors Committee. He is also a recipient of the EMGS 2019 Newly Independent Investigators Engagement Program and is a strong advocate for the mission of the EMGS.
Dr. Maxwell C.K. Leung
University of California, Davis
Dr. Maxwell C. K. Leung is an Associate Toxicologist of the Department of Pesticide Regulation at the California Environmental Protection Agency. He is also an Adjunct Assistant Professor in the Department of Environmental Toxicology at the University of California, Davis. Previously, he was an ORISE Postdoctoral Fellow in the National Center for Computational Toxicology at the U.S. Environmental Protection Agency. He received his Ph.D. in Environmental Toxicology from Duke University in 2012 under the tutelage of Dr. Joel Meyer.
Dr. Leung’s research leverages the power of bioinformatics, computational simulation, in vitro assays, and C. elegans models to examine mitochondrial genotoxicity and health effects over the lifespan. He has published seventeen peer‐reviewed articles and two book chapters, including a comprehensive C. elegans toxicology review that has been cited over 400 times. He is currently studying mitochondrial toxicity as a potential mechanism to disrupt cholesterol, xenobiotic, and testosterone trafficking in spermatogenesis. He is also interested in mitochondria as a toxicity target of cannabis contaminants that result in neurological hazards.
Dr. Leung is a co-chair of the upcoming 2020 EMGS Bioinformatics Challenge. The goal of this competition is to encourage members to work together as an expert community to develop novel tools and approaches that harness publicly available big data to identify signatures of genotoxic hazards. Dr. Leung is also the president-elect of the Genetic and Environmental Toxicology Association of Northern California. As a candidate for the EMGS Council, he looks forward to promoting the interaction between EMGS and different regional societies. He will also continue his effort to recruit student, postdoctoral, and new investigator members in support of mentorship and career development in EMGS.
Dr. Yuan Liu
Florida International University
Dr. Yuan Liu earned her M.D. in Environmental Medicine at Tongji Medical University in China and her Ph.D. in Biochemistry at the University of Rochester School of Medicine and Dentistry with Dr. Robert Bambara. She had her postdoctoral training with Dr. Samuel Wilson at the National Institute of Environmental Health Sciences/NIH. Dr. Liu joined the Department of Chemistry and Biochemistry at Florida International University (FIU) in 2010 and was promoted to a tenured associate professor in 2016.
Dr. Liu is currently the Director of Biochemistry Ph.D. Program at FIU. Dr. Liu’s research focuses on understanding how DNA base damage and base excision repair (BER) can modulate trinucleotide repeat instability and epigenetic features of tumor suppressor genes that are involved in the development of neurodegenerative diseases such as Huntington’s diseases and cancer. Her research aims to discover new targets for prevention, diagnosis, and treatment of the human degenerative diseases. Dr. Liu’s research has established a fundamental paradigm that underlies dynamic changes of DNA repeat sequence through DNA base damage and BER and crosstalk among DNA repair pathways. Her research also has led to the discovery of small molecular compounds as a novel and effective treatment of repeat expansion diseases and the inhibitors of BER enzymes, Pol β and DNA ligase I as new therapy of prostate cancer.
Dr. Liu’s research has led to 60 peer review articles published in the journals of Nature, Nature Communications, Mol Cells, PNAS, Nucleic Acid Research, among others. Her research is supported by NIH R00 and R01 grants. Dr. Liu has served as the reviewers of several NIH study sections and reviewers for over 20 journals. Dr. Liu was the 2012 FIU Top Scholar and awarded the 2016 College of Arts, Sciences and Education (CASE) Research Award and 2018 CASE Service Award.
Dr. Luke Montrose
Boise State University
Dr. Luke Montrose is an environmental toxicologist with research interests in public health, epigenetics, and chronic illness, particularly as it relates to vulnerable and understudied populations.
As an Assistant Professor in the Department of Community and Environmental Health at Boise State University, Dr. Montrose is positioning himself to work collaboratively across campus and across Idaho with relevant stakeholders, including faculty, state and local officials, and community partners. The Montrose Lab leverages expertise in epigenetics, community research, and exposure assessment to better understand the molecular basis of toxicant-induced disease risk throughout the lifecourse.
Dr. Montrose’s research portfolio reflects his passion for studying human health through multiple lenses, ranging from community health to molecular biology. His recent studies have used cutting edge technology to measure exposure-induced epigenetic changes related to diet, air pollution, heavy metals and endocrine disrupting chemicals, and related these changes to humans and animal health effects.
The Montrose Lab aims to translate basic science into practical clinical and community solutions. By studying complex cell and molecular questions in rodent models, complemented by human community based participatory studies, Dr. Montrose elevates the impact that he and his students have on their shared mission of enhancing public health.
Dr. Dan Roberts
Charles River Laboratories
Dan Roberts is a Principal Research Scientist in the Genetic and In Vitro Toxicology Department at Charles River Labs (Skokie) with over 14 years of experience in applied genetic toxicity testing. He received his MS in biotechnology from Johns Hopkins University and obtained Ph.D. Candidacy in the toxicology program at Rutgers University while working full time on his career. Mr. Roberts began his profession at Litron Laboratories as a study director specializing in flow cytometric techniques and then as a Senior Research Associate at Covance Labs where he participated in validating the pig-a gene mutation assay. Following that, Mr. Roberts designed and conducted in vivo and in vitro genetic toxicity assays to evaluate product safety as a Research Scientist at Bristol-Myers Squibb Company, and then as a Principal Scientist at iuvo BioScience. He is former Chairman of the Genetic Toxicology Association and currently co-chairs the New Technologies Special Interest Group (EMGS) and a Genetic Toxicology Committee Working Group (HESI).
Considering this background, Mr. Roberts’ research aim is to integrate new methods into applied genetic toxicity testing paradigms that will enrich our understanding of how chemicals interact with cellular material to induce adverse apical responses. Combined with an adverse outcome pathway, these data will help shape the future of product safety assessment as we will have data identifying molecular initiating events that can inform on DNA-reactivity. Currently, he is focused on applying upstream key events to predict non-covalent DNA interactions and topoisomerase inhibition.
Dr. Laurie Sanders
Laurie H. Sanders, Ph.D. is an assistant professor within the Department of Neurology, a member of the Center for Neurodegeneration & Therapeutics and Duke Cancer Institute at Duke University Medical Center. Dr. Sanders received her Bachelor of Science from Cornell University and Ph.D. degree in biochemistry from the University at Buffalo. She completed her postdoctoral training in the Pittsburgh Institute for Neurodegenerative Diseases at the University of Pittsburgh, during which she was recognized with The First Parkinson’s Action Network Postdoctoral Advocacy Prize. Dr. Sanders also completed a Masters Certificate in Clinical Research through The Institute for Clinical Research Education from the University of Pittsburgh School of Medicine.
In 2015, she was granted the William N. & Bernice E. Bumpus Foundation Innovation award for high risk/high reward ideas that could advance our understanding of Parkinson’s disease. She has established mitochondrial DNA damage and repair as a new area of research in the field of Parkinson’s disease as well as pioneered new technology for measuring mitochondrial DNA integrity.
Dr. Sanders is currently leading multiple human studies with biospecimen and clinical data collection and provides thought leadership for Parkinson’s disease clinical trials. Her translational research focuses on peripheral biomarkers for better diagnosis, treatment and design of clinical trials for Parkinson’s disease. More recently she has discovered a new role for the Parkinson’s disease LRRK2 gene in breast cancer. Her lab is currently pursuing how LRRK2 dysfunction may be at the nexus of both cancer and neurodegeneration, as understanding LRRK2 mechanisms may shed light on both diseases.
Dr. Jeff Wickliffe
Jeffrey K. Wickliffe, Ph.D. is an environmental toxicologist, chemical risk assessor, and exposure scientist by training. His research interests primarily focus on genetic toxicology and the chemical and physical agents that cause genetic damage and contribute to mutagenesis. He has worked on developing and applying biomarkers of DNA damage and exposure such as DNA adduct detection and quantification as well as biomarkers of exposure and effect such as mutation biomarkers including HPRT/Hprt and PIG-A/Pig-a gene mutations.He has investigated exposures and mutational effects in human cohort studies, controlled animal studies under laboratory conditions and under field-deployed conditions, and using in vitro methods in mammalian cells. He has also used transgenic animals models for mutational analysis.
Dr. Wickliffe has been an active, full member of EMGS since 2008 but began attending the annual meeting in 2001 as a pre-doctoral student. He has served on, and been chair of, the Public Relations and Communications Committee. He has also chaired and co-chaired the Environmental Genetic Toxicology Special Interest Group.
The ballot will close on December 27, 2019.