Program - Society of Toxicology

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44 th Annual Meeting and ToxExpo Program Description MONDAY #342 12:45 INTRACARDIAC AND INTRAVASCULAR LEAD UTILIZATION: METHODS FOR IMPROVED DATA COLLECTION. C. Hassler. Safety Pharmacology, Battelle Memorial Laboratories, Columbus, OH. Sponsor: L. Kinter. #343 1:00 OBTAINING QUALITY ECG ENDPOINTS IN SAFETY PHARMACOLOGY AND GENERAL TOXICOLOGY STUDIES. ARE RESTRAINT AND SURGICAL INTERVENTION NECESSARY? M. Zawada and L. B. Kinter. Safety Assessment, AstraZeneca, Wilmington, DE. Abstract 344 is located on page74. Monday Afternoon, March 7 1:30 PM to 4:30 PM Room RO8 INNOVATIONS IN TOXICOLOGICAL SCIENCES SESSION: ALTERNATIVE RNA SPLICING: A MECHANISM FOR ENHANCING DIVERSITY OF GENE EXPRESSION Chairperson(s): Curt Omiecinski, Pennsylvania State University, University Park, PA and Craig Marcus, University of New Mexico, Albuquerque, NM. Endorsed by: Carcinogenesis SS Alternative RNA splicing is an emerging field of molecular science that has significant impact on the toxicological considerations of gene expression and protein function. The diversity of alternatively spliced transcripts has farreaching significance in terms of understanding interindividual differences in response to xenobiotics, mechanisms of toxicity at the molecular level, tissuespecific toxicity, and the mechanisms for regulating responses to environmental and chemical challenge. This Symposium will provide an overview of basic mechanisms and toxicological significance of RNA alternative splicing, with a focus on alternatively spliced xenobiotic nuclear receptors. Importantly, the session will also address bioinformatics-related issues pertaining to the identification of splice variants, including the design of microarray and genomics platforms that facilitate variant transcript detection. #286 1:30 INTRODUCTION TO SYMPOSIUM: ALTERNATIVE RNA SPLICING: A MECHANISM FOR ENHANCING DIVERSITY OF GENE EXPRESSION. C. Omiecinski. Ctr Molec Toxicology, Penn State University, University Park, PA. #287 1:35 DISCOVERY AND TISSUE-SPECIFIC MONITORING OF ALTERNATIVE PRE-MNRA SPLICING WVENTS USING INK-JET MICROARRAYS. J. M. Johnson, J. Castle, P. Garrett- Engele, Z. Kan, L. Lim, C. Armour, C. Raymond and E. Schadt. Informatics, Rosetta Inpharmatics, Merck & Co., Inc., Seattle, WA. Sponsor: C. Marcus. #288 2:10 FUNCTIONALLY DISTINCT ISOFORMS OF THE FARNESOID X RECEPTOR (FXR). P. A. Edwards, Y. Zhang and F. Y. Lee. Biological Chemistry, UCLA, Los Angeles, CA. Sponsor: C. Marcus. #289 2:45 HUMAN PXR: GENERATION OF DIVERSITY THROUGH ALTERNATIVE SPLICING AND POLYMORPHISM. E. G. Schuetz. Pharmaceutical Sciences, St. Jude Children’s Research Hospital, Memphis, TN. Sponsor: C. Marcus. #290 3:20 FUNCTIONALLY DISTINCT ALTERNATIVE SPLICE VARIANTS OF THE HUMAN XENOBIOTIC RECEPTOR, CAR. C. Omiecinski, S. Auerbach and M. Stoner. Ctr Molec Toxicology, Penn State University, University Park, PA. #291 3:55 STEROID RECEPTOR COACTIVATORS PROMOTE COORDINATE TRANCRIPTION AND ALTERNATIVE SPLICING. B. W. O’Malley. Molecular & Cellular Biology, Baylor College of Medicine, Houston, TX. Sponsor: C. Marcus. Monday Afternoon, March 7 1:30 PM to 4:30 PM Room 208 SYMPOSIUM SESSION: DIETARY ACRYLAMIDE: NEW OR ANCIENT RISK? Chairperson(s): Philip M. Bolger, U.S. FDA, College Park, MD and Danial Doerge, National Center for Toxicological Research, Jefferson, AR. Endorsed by: Food Safety SS* Occupational and Public Health SS Regulatory and Safety Evaluation SS Risk Assessment SS Initial investigations by Swedish researchers of fried and oven-baked foods indicated that acrylamide formation is associated with high temperature cooking processes for certain carbohydrate-rich foods, such as potatoes and cereals. Since then similar findings have been reported by researchers in other countries. The discovery of acrylamide in food is a concern because acrylamide is a potential carcinogen and genotoxicant, and a known human neurotoxicant. It does not appear to be present in uncooked food and is present in low or undetectable levels in foods cooked at lower temperatures, such as by boiling. One plausible mechanism responsible for acrylamide formation in carbohydrate-rich foods cooked at high temperatures is the Mallard reaction between asparagine and certain sugars. However, not enough is known about acrylamide formation to identify safe, effective, and practical modifications to food processing techniques that will clearly prevent or reduce formation. Identifying major mechanisms of formation is an important step in identifying ways to reduce or prevent acrylamide formation during cooking. There are significant uncertainties about the impact of dietary acrylamide exposure on public health, since foods reported to contain acrylamide have been consumed for many years. While acrylamide causes cancer in laboratory animals at high doses, it is not clear whether a similar response would occur at the much lower levels found in food. Several epidemiological environmental studies of workplace and dietary exposures have failed to show an increased cancer risk with acrylamide exposure. It is also conceivable that subtle effects can occur on the developing nervous system at acrylamide doses lower than those that have been studied in animals and humans. To better assess the risk of acrylamide information is needed on dietary exposure, bioavailability from food, biomarkers of exposure, and the potential to cause cancer and neurotoxic or neurodevelopmental effects when consumed in food. #292 1:30 OVERVIEW OF DIETARY ACRYLAMIDE. P. M. Bolger. Center for Food Safety and Applied Nutrition, US Food and Drug Administration, College Park, MD. #293 1:35 TOXICOKINETICS OF ACRYLAMIDE AND GLYCIDAMIDE IN B6C3F1 MICE AND FISCHER 344 RATS. D. R. Doerge 1 , J. F. Young 2 , L. McDaniel 1 , N. C. Twaddle 1 and M. I. Churchwell 1 . 1 Biochem. Toxicol., NCTR, Jefferson, AR and 2 Biometry and Risk Assessment, NCTR, Jefferson, AR. Sponsor: P. Bolger. 70 SOT’s 44 th Annual Meeting
44 th Annual Meeting and ToxExpo Program Description #294 1:50 REFERENCE VALUES IN THE ACRYLAMIDE IRIS ASSESSMENT DEVELOPED BY THE U.S. EPA. R. S. DeWoskin. ORD/NCEA, U.S. EPA, Research Triangle Park, NC. #295 2:30 DIETARY ACRYLAMIDE AND RISK OF HUMAN CANCER: THE ROLE OF EPIDEMIOLOGY. L. Mucci 1 and H. Adami 2 . 1 Channing Laboratory, Harvard Medical School, Boston, MA and 2 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Sponsor: P. Bolger. #296 3:10 AN INTERNATIONAL SAFETY/RISK ASSESSMENT OF ACRYLAMIDE. S. H. Henry. Center for Food Safety & Applied Nutrition (HFS-308), U. S. Food & Drug Admin., College Park, MD. Monday Afternoon, March 7 1:30 PM to 4:30 PM La Louisiane Ballroom B SYMPOSIUM SESSION: ENVIRONMENTAL FACTORS AFFECTING BREAST CANCER SUSCEPTIBILITY Chairperson(s): Suzanne Fenton, U.S. EPA, Research Triangle Park, NC and Scott W. Burchiel, University of New Mexico, Albuquerque, NM. Endorsed by: Carcinogenesis SS Reproductive and Development SS* Toxicologic and Exploratory Pathology SS Women in Toxicology SS Breast cancer is still the most common malignancy afflicting women in the Western world. Although substantial progress has been made in elucidating some of the genetic contributors to breast cancer (i.e., the highly penetrant susceptibility genes, BRCA1 and 2), it has been estimated that only 6-12% of all breast cancer cases are due to heritable factors. Few other specific factors have been identified that contribute significantly to an individuals lifetime risk of breast cancer. It has become apparent that elements affecting cancer susceptibility (genetic or environmental components) cannot be considered separately. Environmental factors (e.g., industrial compounds, pharmaceuticals, diet, occupational hazards) have been identified in both epidemiological and rodent studies that alter breast development and tumor formation. These constituents may act as either a mutagen or as a developmental compound able to alter susceptibility to carcinogens. In addition to the contributions of environmental factors, a large percentage of cancer cases are due to sporadic mutations that may occur as a result of spontaneous genetic events, and the interactions between gene and environmental factors. A relatively recent focus in the breast cancer field is on the interaction between genes and environment as the causal mechanism in the disease. Primary candidates for gene-environment interaction studies have been genes that encode enzymes involved in the metabolism of established cancer risk factors and those involving oxidative stress response. There are common varying forms of these genes (polymorphisms) that may directly result in impacting the risk of cancer by altering normal metabolism, circulating hormone levels, ability to respond correctly to normal stressors, or response to environmental factors. We will present data from both epidemiological and rodent studies demonstrating the importance that environmental factors play in breast cancer susceptibility. These studies will elucidate the importance of evaluating gene-environment interactions and the various environmental factors, such as diet and endocrine disrupting chemicals, on breast cancer risk assessment. #297 1:30 ENVIRONMENTAL FACTORS AFFECTING BREAST CANCER SUSCEPTIBILITY. S. Fenton. U.S. EPA, Research Triangle Park, NC. #298 1:45 GENE-ENVIRONMENT INTERACTIONS IN THE ETIOLOGY OF BREAST CANCER. C. Ambrosone. Roswell Park Cancer Institute, Buffalo, NY. Sponsor: S. Fenton. #299 2:15 INFLUENCE OF ENDOCRINE DISRUPTING COMPOUNDS (EDCS) ON MAMMARY GLAND DEVELOPMENT AND TUMOR SUSCEPTIBILITY. S. Fenton 1 and J. L. Rayner 2 . 1 Reproductive Toxicology Division, U.S. EPA, Research Triangle Park, NC and 2 DESE, UNC, Chapel Hill, NC. #300 2:45 EARLY LIFE DIETARY ESTROGENIC EXPOSURES AND LATER SUSCEPTIBILITY TO MAMMARY TUMORIGENESIS. L. A. Hilakivi- Clarke, B. Yu and M. Martin. Oncology, Georgetown University, Washington, DC. Sponsor: S. Fenton. #301 3:15 DNA DAMAGE/REPAIR IN HUMAN BREAST CANCER RISK. J. J. Hu. Cancer Biology, Wake Forest U. School of Medicine, Winston-Salem, NC. #302 3:45 ROLE OF OXIDANT STRESS IN THE ACTIVATION OF GROWTH FACTOR SIGNALING PATHWAYS IN HUMAN BREAST EPITHELIAL CELLS BY ENVIRONMENTAL POLYCYCLIC AROMATIC HYDROCARBONS (PAHS). S. W. Burchiel 1 , A. D. Burdick 2 , K. F. Melendez 1 , F. T. Lauer 1 and J. W. Davis 3 . 1 College of Pharmacy, University of New Mexico, Albuquerque, NM, 2 Center for Molecular Toxicology, Penn State University, University Park, PA and 3 Worldwide Safety Sciences, Pfizer Global Research and Development, St. Louis, MO. MONDAY up-to-date information at www.toxicology.org 71
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Annual Meeting Events Calendar (Con
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Program - Society of Toxicology

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