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March 1, 2018 | 12:30 p.m. - 1:30 p.m.
Category: Seminar
Location: Integrative Biosciences Center 1D
Cost: Free
Audience: Academic Staff, Alumni, Community, Current Graduate Students, Current Undergraduate Students, Faculty, Parents, Prospective Students, Staff

The Center for Urban Responses to Environmental Stressors (CURES) presents their Thursday afternoon seminar series on March 1, 2018 from 12:30 to 1:30 p.m. at the IBio Building in Seminar Room 1D, located at 6135 Woodward Ave.  The seminars are free and open to the entire university community.

The guest speaker will be Shuk-Mei Ho, Ph.D., director of the Cincinnati Cancer Center (CCC), associate dean for Basic Research at the University of Cincinnati and president, UC Physicians' Environmental and Occupational Health Unit. Dr. Ho will present, " Environmental Epigenetics, Stem Cell Reprogramming, and Transgenerational Health Effects."

Dr. Ho received a Bachelors of Science in Biological Sciences (1st Class Honor) and a Doctorate degree in Zoology from the University of Hong Kong.  Dr. Ho's current research focus is on epigenetic mechanisms in epidemiological studies.  Utilizing state-of-the-art investigative tools and technology for genomics, transcriptomics, proteomics, epigenomics and informatics, Dr. Ho's work explores the effects of multi-environmental exposures at various developmental stages and the transgenerational consequences of exposure on epigenetic changes in relation to cancer susceptibility.  Her findings have implicated epigentic dysregulation of gene-expression associated with early-life exposure to toxic compounds as a root cause of later development of cancers, asthma, cardiometabolic disorders and other complex chronic diseases.

ABSTRACT

It is now known that many environmental toxicants associated with chronic complex diseases are not genotoxic; they do not cause mutations or chromosomal changes.  Instead, they exert their actions through epigenetic modifications of the genome, altering the gene expression patterns of susceptible cells or organs.  A prime example is the plasticizer, bisphenol A (BPA). Early-life exposure of rats to BPA altered their prostate epigenome and increased prostate cancer risk in adult life, in a non-linear dose-dependent manner.  The exposure induces permanent dysregulations in gene expression of target cells via long-lasting epigenetic reprogramming.  Of interest, the stem cells in the prostatic epithelium are affected with regard to cell fat, pluripotency, signaling mechanisms and differentiation in this animal model.  Similar scenarios were observed for mammary glands, the endometrium and specific brain areas.  Extending to human studies, other environmental pollutants including traffic-related pollutants (polycyclic aromatic hydrocarbons, diesel exhaust) and dietary contaminants (methylmercury, PCBs, pp-DDE, hexachlorobenzene, and perfluoroalkyl substances) have been shown to induce epigentic changes at varying degrees, in cord blood of infants, buccal cells of children, and adult blood DNA.  The epigenetic changes often serve as biomarkers or sentinels for disease development in the target organs associated with chronic illnesses such as asthma, reproduction disruption, and aberrant neurobehavioral disorders.  Although DNA methylation was found to be a significant eigenomic mechanism for reprogramming of disease risk, histone modifications, alteration of non-coding RNA expression, and other higher chromatin changes play equally important roles.  Future research focusing on transgenerational environmental epigenomic changes and disease risk changes over generations will advance the field of precision disease prevention.

For more information about this event, please contact Christina Cowen at 313-577-6590 or mzchris@wayne.edu.