Archive of All Young Scientist Award Videos

EMGS Young Scientist Award Submissions

Environmental Mutagenesis and Genomics Society

Ever wonder what things in the environment do to your genes? We are the Environmental Mutagenesis and Genomics Society (EMGS), scientists in academia, government, and industry working to understand the genetic impacts of environmental exposures to promote human health. Through research we learn how genes in your body respond to the environment, how changes impact health and get passed to your children, and what we should do about this.

EMGS Young Scientist Award

EMGS is committed to helping young scientists - our future - make critical career transitions. At our Annual Meeting, we feature the EMGS Young Scientist Award, a chance for a new investigator embarking on an independent scientific career to give a plenary talk. Don't underestimate this honor! Face-to-face communication is one of the most important ways we learn, network, and make our science better.


Laurie Sanders: is an assistant professor at Duke University School of Medicine in the department of Neurology. Her current research pursues  the  novel  hypothesis  that defective  maintenance  of  genome  integrity  is  an  upstream  mechanism contributing to the progressive neurodegeneration that occurs in PD. To summarize her lab’s recent findings, they observed that in addition to mtDNA damage,mutant LRRK2 induces nuclear DNA double-strand breaks (DSBs) and the ATM-mediated DNA damage response. PD-linked LRRK2mutations confer a vulnerability in response to DSB damaging agents by further exacerbating genome  instability,  resulting in cell  death.  They  found  mutant  LRRK2 kinase  activity  modulates  ATM  substrates, suggesting  that  mutant  LRRK2  is upstream  of  ATM signaling. Their results  support  the  notion  of  an unanticipated  role  for LRRK2 in genome maintenance and the DNA damage response. She is also interested in novel clinical trial design and how best to integrate biomarkers into PD clinical trials and provides thought leadership relevant to PD and age-related neurodegenerative diseases clinical trials. She serves as a key opinion leader in the PD space for protocol and clinical trial design and hopes to have a broader impact on PD research and therapeutics through this capacity.

Jennifer Mason: is an assistant professor at Clemson University, Department of Genetics and Biochemistry. Her research efforts focus on (1) understanding the non-enzymatic roles of the central HR recombinase, RAD51 at stalled replication forks and (2)understanding how proteins that regulate RAD51 activity function at replication forks. One current project focuses on the RAD54 translocases, RAD54L and RAD54B. Her lab studies the molecular mechanisms that maintain replication fork integrity during times of stress. They use human cancer cell models to study the biological consequences of targeted mutations in DNA repair genes on the replication stress response and to better understand the function of DNA repair proteins at stalled replication forks. Currently, they use a combination of biochemical, cell, and molecular biology approaches to study the role of proteins that function within the homologous recombination pathway (HR). Her work will lead to a better understanding of the replication stress response in human cells and determine how loss of this pathway results in genome instability and cancer predisposition.

Jennifer Kay: is currently a postdoctoral research fellow in Dr. Bevin Engelward’s lab at the Massachusetts Institute of Technology, Department of Biological Engineering.  Her current research is in evaluating how genetic factors impact susceptibility to mutations and cancer following exposure to N-nitrosodimethylamine (NDMA), a chemical that contaminates the groundwater of Wilmington, MA due to irresponsible waste disposal at the Olin Chemical Superfund site. While work has been done to remediate the site and to replace contaminated well water with municipal water, NDMA contamination persists, and residents living near the Olin Chemical Superfund Site remain highly concerned. Following completion of her postdoctoral training, she will be transitioning to an independent investigator role with the non-profit Silent Spring Institute in Newton, MA. She hopes to contribute to community-based participatory environmental health research, development of Adverse Outcome Pathways, and engagement with government scientists and regulators responsible for environmental and public health policies.

Jackie Goodrich: is a research assistant professor at the University of Michigan School of Public Health, in the department of Environmental Health Sciences. The overarching goal of Dr. Goodrich’s research is to identify environmental factors that modify the epigenome and increase risk for disease throughout the lifecourse. Her research addresses prominent public health issues by investigating associations between pervasive toxicants and risk for chronic diseases via epigenetic mechanisms. A substantial focus of her research program is on children’s health and the Developmental Origins of Health and Disease (DOHaD). She is especially interested in prenatal and early childhood exposures that modify epigenetic programming and their subsequent impacts on fetal and child growth, risk for obesity, and metabolic complications later in life. The other major arm of her research program focuses on the health effects of occupational exposures with epigenetic perturbation as a biomarker of or mechanism underlying these effects. Her ongoing and future research is aimed at evaluating the effects of emerging environmental exposures (e.g., PFAS) on the most vulnerable populations – children, pregnant women, and workers.


Zachary Nagel: The overarching theme of Dr. Nagel's research is to bring detailed, mechanistic cellular and molecular-level tools and expertise to bear on problems in public health and cancer therapy.  In particular, he is interested in the health effects of environmental and medical exposures to radiation and other DNA damaging agents, with emphasis on the lung and blood.  His research falls under two interrelated areas of focus: Molecular Epidemiology of the Health Effects of DNA Damage and Mechanisms of DNA Damage and Repair in Cancer Development and Treatment.

Elise Fouquerel: The overarching goal of Dr. Fouquerel's research is to decipher the roles played by Poly(ADP-ribose) polymerases (PARPs) in the maintenance of genome stability. PARP1 is a key component of the cellular stress response, and functions as both a stress sensor and response mediator. Cellular stress can arise from various intrinsic and extrinsic sources including exposure to numerous environmental agents (i.e. ultraviolet light, oxidants, alkylating chemicals, etc.), and can include the generation of DNA damage, mutations and DNA replicative stress. Stress responses can trigger pathological conditions including inflammatory diseases, metabolic dysregulation, accelerated aging and cancer. Notably, epidemiological studies show that more than 20% of all cancers are caused by chronic inflammation associated with oxidative stress. PARP1 activity is involved in the cellular fate decision of survival or death, depending on the stress severity. In this regard, PARP1 inhibitors are being developed as therapeutics for different cancers, mainly for DNA repair deficient tumors in a context of synthetic lethality.


Aishwarya Prakash: Dr. Aishwarya Prakash began her independent research career as a tenure-track Assistant Professor at the University of South Alabama Mitchell Cancer Institute (MCI) in March 2016. My primary passion as a structural biologist is to obtain high-resolution, three-dimensional structures of DNA repair complexes via X-ray crystallography. DNA repair pathways are necessary to protect the human genome from constant assault from a variety of exogenous (ionizing radiation, cigarette smoke etc.) and endogenous factors (such as ATP generation via normal respiration). My laboratory is interested in two DNA repair pathways: the base excision repair (BER) pathway, which is involved in the repair of small, non-bulky DNA lesions and the mismatch repair (MMR) pathway, which is
involved with recognizing and removing erroneous DNA base misincorporations, insertions, and deletions. Both BER and MMR are highly conserved, sequential processes that rely on the formation of productive protein-DNA or protein-protein complexes to recognize, remove, and replace the damage, which ultimately results in damage-free, repaired DNA.

Isabelle Miousse: Dr. Isabelle Racine Miousse is a postdoctoral fellow in Occupational and Environmental Health at the University of Arkansas for Medical Sciences. She received her Ph.D in Human Genetics from McGill University in Canada studying the metabolism of vitamin B12, a cofactor in the methionine cycle. Dr. Miousse is author/co-author of over 38 peer-reviewed articles. Her work focuses on epigenetic toxicology, and particularly on the regulatory effect of the metabolism of methionine and methyl groups after environmental exposures.

Mark Hedglin: Dr. Mark Hedglin is a Assistant Professor at the Pennsylvania State University. He currently focuses on three major topics; Human Okazaki Fragmentation synthesis, Translesion DNA synthesis by Replicative DNA polymerases, and Chromatin assembly at sites of DNA damage.

Matt Schellenberg: Topoisomerase 2 (TOP2) is essential for life, and alters DNA topology via formation of the TOP2 cleavage complex (TOP2cc), a covalent enzyme-­DNA reaction intermediate where a DNA double-­strand break (DSB) is maintained by a covalent linkage between a TOP2 active-­site tyrosine and DNA 5′-­phosphate. TOP2cc is vulnerable to trapping by environmental toxicants, chemical metabolites, damaged DNA and repair intermediates, and precisely targeted with potent, front-­line anticancer TOP2 drugs such as etoposide and doxorubicin that trap or “poison” TOP2cc, resulting in highly genotoxic “dirty” DSBs with ends blocked by a DNA-­Protein Crosslink (TOP2-­DPC, Fig. 1). TOP2-­DPC repair factors must be able to efficiently distinguish between normal reaction intermediates (TOP2cc) and poisoned TOP2 (TOP2-­DPCs), and remove the covalently linked TOP2 protein molecules so the DNA break can be rejoined by DNA ligases

Natalie Gassman: The Gassman lab is using novel confocal fluorescent techniques to study DNA damage induction (adductomics) and alterations in DNA damage response and repair, as a function of cell line background (micro-irradiation) and co-exposure with environmental and therapeutic DNA damaging agents (altered cytotoxicity and chemotherapuetic activity). This work has lead to the development of a novel DNA damage assay and provided new insight into the functions of DNA repair proteins at sites of induced DNA damage. Our long term goals are a better understanding of how DNA repair defects accumulate in cells from exposure and co-exposure and how these defects contribute to the development of cancer and to its treatment.

Melike Caglayan: Both human-made toxicants and naturally occurring toxins in the environment can damage genomic DNA and promote deleterious DNA damage and DNA damage responses. This negative cellular impact is prevented by DNA repair, and in the case of repair failure toxic consequences can occur. Base excision repair (BER) is a key DNA repair process responsible for repairing cytotoxic and mutagenic base lesions and strand breaks that if not corrected can lead to deleterious mutations, genomic instability, or cell death. The multi-step BER pathway is coordinated by channeling of DNA intermediates between the gap filling DNA synthesis step by DNA polymerase β (pol β) and the ligation step by DNA ligases. This hand-off is important to prevent the release of toxic repair intermediates in cells. My research focus is on understanding of how environmental agents impact downstream steps in the base lesion DNA repair pathway and the biochemical mechanism and cytotoxic effects of failure in the ligation step of the DNA repair process, especially when compromised by environmental oxidant-induced effects.

Shobhan Gaddameedhi:

Yunfeng Lin:


Bogdan Fedeles: is a research scientist at Massachusetts Institute of Technology, in the department of Biological Engineering and Center for Environmental Health Sciences (CEHS), working in the lab of the CEHS director Dr. John Essigmann. The overarching goal of Dr. Fedeles’ research is to develop a unified framework for decoding the mutational records of cells, which would enable early cancer diagnosis, better exposure risk assessment and insights into disease etiology. To study mutagenesis, Dr. Fedeles utilizes a multidisciplinary approach, which includes biological chemistry to construct site-specific nucleic acid lesions and analogs, chemical and spectroscopic tools to study lesion biochemistry, and molecular biology and genetics experiments to assess the contribution of the genetic background to mutagenic outcomes. His current work investigates the mutagenic consequences of inflammation, and their contribution to the mutational burden observed in many inflammation-dependent human cancers. 

Natalie Saini: is currently a postdoctoral scientist in Dr. Dmitry Gordenin’s lab at the National Institute of Environmental Health Sciences.  She is working towards establishing herself as an independent researcher in the near future.  Dr. Saini’s overarching research goal is to determine the range of genome-wide mutation loads and to identify the mutation signatures in the cells of healthy individuals to decipher environmental and genetic causes of genome instability.  She utilizes simple model organisms like yeast to understand how environmental agents affect DNA stability, and to apply this knowledge in more complex human research.  Her combinatorial approach enables her to answer key questions regarding the impact of environmental damage on mutagenesis in humans, resulting in important insights into how these factors affect human health.

Nikolai Chepelev: has developed strong and diverse expertise in toxicogenomics during postdoctoral training at the Genomics Laboratory of Health Canada, led by Dr. Carole Yauk. For this work, he has received three awards: two from Risk Assessment Specialty Section of the Society of Toxicology (e.g., Best Published Paper Advancing the Science of Risk Assessment - 2015) and one from the Environmental and Molecular Mutagenesis (EMM; New Investigator Best Paper Award - 2016). Nikolai showed how toxicogenomics can benefit health risk assessment by providing mechanistic information to explain neurotoxicity and carcinogenicity of benzo[a]pyrene as an example. He has recently joined Genetic Toxicology Laboratory at Health Canada (Leader - Dr. Paul White), where he is applying both traditional toxicity tests (bacterial mutagenicity and transgene mutation assays) and toxicogenomics. His goal is to develop high-throughput platform for in vitro Genetic Toxicity Assessment of chemicals that will rely on both traditional and emerging technologies. These efforts will facilitate our movement towards improved 21st century approaches in toxicology and health risk assessment.

Ludmil Alexandrov: completed his PhD in 2014 at the University of Cambridge and since then he has been an Oppenheimer Fellow in Theoretical Biology at Los Alamos National Laboratory. Ludmil’s research has been focused on understanding the mutational processes in human cancer through the use of mutational signatures. Ludmil developed the first comprehensive map of mutational signatures in human cancer and demonstrated the applicability of mutational signatures to cancer prevention and cancer treatment. Ludmil has more than 55 publications in well-respected scientific journals and he has won multiple awards for his work on mutational signatures, including:  listed as “30 brightest stars under the age of 30” by Forbes magazine; a Harold M. Weintraub Award by the Fred Hutchinson Cancer Center; Prize for Young Scientists in Genomics and Proteomics by Science magazine; Carcinogenesis Young Investigator Award by European Association for Cancer Research. Ludmil is currently one of six co-investigators leading the Mutographs of cancer, a project that seeks to understand the unknown cancer-causing factors across the globe by examining mutational signatures from 5,000 cancer patients from 17 countries across five continents


Bret Freudenthal::

Nikolai Chepelev: