Program - Society of Toxicology
Program - Society of Toxicology
Program - Society of Toxicology
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<strong>Society</strong> <strong>of</strong> <strong>Toxicology</strong> 2011<br />
<strong>Program</strong> Description (Continued)<br />
Abstract #<br />
#1768 6:30 FROM PILOT GRANTS TO HIGH-END<br />
JOURNALS: THE SCIENCE OF WRITING, <br />
M. C. Fortin 1 and A. E. Loccisano 2 . 1 Clinical<br />
Research and Occupational Medicine, Environmental<br />
and Occupational Health Sciences Institute,<br />
Piscataway, NJ and 2 The Hamner Institutes for<br />
Health Sciences, Research Triangle Park, NC.<br />
6:30 Introduction. Marie Fortin<br />
6:34 Communicating Ideas Efficiently: An Essential<br />
Skill for All Researchers. Deborah A. Cory-<br />
Slechta<br />
6:53 Grantsmanship at NIH: How to Swim with the<br />
Sharks. Jerrold J. Heindel<br />
7:12 Writing for Success. Angela K. Eggleston<br />
7:31 Panel Discussion/Q&A.<br />
Wednesday Morning, March 9<br />
8:00 AM to 9:00 AM<br />
Grand Ballroom<br />
Keynote Medical Research Council (MRC)<br />
Lecture: Cellular Responses to DNA Damage:<br />
New Molecular Insights and New Approaches<br />
for Cancer Therapy<br />
Lecturer: Stephen P. Jackson, The Gurdon Institute<br />
and Department <strong>of</strong> Biochemistry, University <strong>of</strong><br />
Cambridge, Cambridge, United Kingdom.<br />
Inherited or acquired defects in detecting, signalling or repairing DNA<br />
damage are associated with various human pathologies, including<br />
immuno-deficiencies, neurodegenerative diseases and various forms <strong>of</strong><br />
cancer1. Our increasing knowledge <strong>of</strong> cellular DNA-damage responses<br />
(DDR) is therefore providing new insights into the aetiology <strong>of</strong> such<br />
diseases and, moreover, is presenting opportunities for novel diagnostic<br />
and therapeutic strategies. Work in Dr. Jackson’s laboratory aims to<br />
decipher the mechanisms by which cells detect DNA damage and signal<br />
its presence to the DNA-repair and cell-cycle machineries. In particular,<br />
much <strong>of</strong> the work focuses on DNA double-strand breaks (DSBs) that are<br />
generated by ionizing radiation and radiomimetic chemicals, and which<br />
can also arise when the DNA replication apparatus encounters other<br />
DNA lesions.<br />
In this talk, Dr. Jackson will first provide an overview <strong>of</strong> how cells<br />
respond to DNA damage and will describe the key protein players in<br />
these events. Next, he will discuss some <strong>of</strong> our recent work that has<br />
identified new proteins that mediate DSB responses, control DSB<br />
processing or modulate chromatin structure at DNA damage sites. He<br />
will then explain how this type <strong>of</strong> work identified therapeutic opportunities<br />
that led to me founding KuDOS Pharmaceuticals Ltd, whose<br />
mission was to develop DDR inhibitors for cancer therapy. Finally, He<br />
will use the example <strong>of</strong> the KuDOS drug olaparib (now owned by and<br />
being developed by AstraZeneca) to highlight the exciting potential for<br />
DDR inhibitors in treating many cancers. Specifically, Dr. Jackson will<br />
explain the molecular basis for how olaparib is exquisitely cytotoxic to<br />
cancer cells bearing DSB repair defects because <strong>of</strong> inherited mutations<br />
in BRCA1 or BRCA2 but is well tolerated by normal cells <strong>of</strong> cancer<br />
patients. In closing, he will explain how this and related mechanisms <strong>of</strong><br />
“synthetic lethality” might be applied to a wider range <strong>of</strong> cancers that<br />
bear DDR defects.<br />
Abstract #<br />
Wednesday Morning, March 9<br />
9:00 AM to 11:45 AM<br />
Room 202A<br />
Symposium Session: Autism: Genetic, Epigenetic, and<br />
Environmental Factors Influencing Neural Networks<br />
Chairperson(s): Isaac Pessah, University <strong>of</strong> California Davis, Davis, CA,<br />
and Cindy Lawler, National Institute <strong>of</strong> Environmental Health Sciences,<br />
Durham, NC.<br />
Sponsor:<br />
Neurotoxicology Specialty Section<br />
Endorsed by:<br />
Reproductive and Developmental <strong>Toxicology</strong> Specialty Section<br />
Risk Assessment Specialty Section<br />
Our current knowledge about how genetic, epigenetic, and environmental<br />
factors contribute to autism susceptibility is ever changing. From a toxicologist’s<br />
perspective, the identity <strong>of</strong> defective genes and signaling pathways<br />
linked to autism provide important clues about exposures to environmental<br />
chemicals that influence autism susceptibility, severity, and/or treatment<br />
outcomes. One fundamental way by which heritable genetic vulnerabilities<br />
can amplify the adverse effects triggered by environmental exposures is<br />
if both factors (genes x environment) converge to dysregulate the same<br />
signaling systems at critical times <strong>of</strong> development. Thus, we will review<br />
current knowledge <strong>of</strong> genetic contributions to autism risk, and present new<br />
evidence that autism is associated with an appreciably increased level <strong>of</strong><br />
genomic instability in low copy repeat (LCR) rich intervals <strong>of</strong> the genome<br />
and how environmental factors that affect genomic stability could contribute<br />
to the incidence and severity <strong>of</strong> autism. We will highlight new findings from<br />
both a mouse model <strong>of</strong> Rett Syndrome and human tissues that contribute to<br />
our understanding <strong>of</strong> how developmental exposures to brominated flame<br />
retardants (PBDEs) influence DNA methylation and neurobehavioral<br />
outcomes relevant to autism. An update will be provided on recent progress<br />
in understanding how impairments in neural connectivity contribute to<br />
autism including seminal findings <strong>of</strong> the role <strong>of</strong> MET polymorphisms play<br />
in autism risk and how polyaromatic hydrocarbons found in air pollution<br />
might influence MET signaling. Finally, we will review the major translational<br />
issues confronting autism research and provide information about<br />
current funding opportunities in autism research.<br />
#1769 9:00 AUTISM: GENETIC, EPIGENETIC,<br />
AND ENVIRONMENTAL FACTORS<br />
INFLUENCING NEURAL NETWORKS. I. N.<br />
Pessah. Department <strong>of</strong> Molecular and Biological<br />
Sciences, University <strong>of</strong> California Davis, Davis, CA.<br />
9:00 INTRODUCTION. Isaac Pessah<br />
#1770 9:15 COPY NUMBER BURDEN ASSOCIATED<br />
WITH AUTISM IN UNSTABLE SEGMENTS<br />
OF THE GENOME. S. B. Selleck 1,2,7 , R. L.<br />
Johnson 2 , J. Balciuniene 7,3 , C. M. Conboy 7 , T. B.<br />
Nauth 2 , A. N. Klossner 7 , M. Alsagabi 4 , A. Alqallaf 4 ,<br />
R. Davis 5 , R. Hansen 5 , J. Gregg 5 , I. Hertz-PIcciotto 5 ,<br />
A. Tewfik 4 and I. N. Pessah 6,5 . 1 Biochemistry<br />
and Molecular Biology, The Pennsylvania State<br />
University, University Park, PA, 2 Pediatrics,<br />
University <strong>of</strong> Minnesota, Minneapolis, MN,<br />
3<br />
Biology, Temple University, Philadephia, PA,<br />
4<br />
Electrical Engineering and Computer Science,<br />
University <strong>of</strong> Minnesota, Minneapolis, MN, 5 The<br />
Medical Investigations <strong>of</strong> Neurodevelopmental<br />
Disorders Institute, University <strong>of</strong> California,<br />
Davis, Sacramento, CA, 6 Department <strong>of</strong> Molecular<br />
Biosciences, School <strong>of</strong> Veterinary Medicine,<br />
University <strong>of</strong> California Davis, Davis, CA and<br />
7<br />
Genetics Cell Biology and Development, University<br />
<strong>of</strong> Minnesota, Minneapolis, MN.<br />
Wednesday<br />
Poster Sessions<br />
Regional Interest Session<br />
Roundtable Sessions<br />
Symposium Sessions<br />
Thematic Sessions<br />
Workshop Sessions<br />
273