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For years scientists have known that biological fate is not regulated solely by DNA sequence – super ordinate regulatory mechanisms exist and contribute to determine the function of genes. Intense research has shown that these mechanisms broadly defined as Epigenetics are multifaceted and complex. This conference aims to highlight recent technologies profiling the key molecular players of histone modification and DNA methylation from regulation in normal embryogenesis through changes in epigenetic state that plays a central role in disease. Understanding this regulation can lead to biomarker identification for monitoring drug effects, toxicity and effective dose for therapeutic intervention as well as diagnostic and prognostic tools for disease.
MONDAY, MARCH 15, 2010
8:30 am Short Course Registration
9:00 – 12:00 pm Pre-Conference Short Courses*
Click here for the complete short course descriptions.
* Separate Registration Required
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1:00 pm Conference Registration
2:00 Chairperson’s Remarks
Michelle Barton, Ph.D., Professor, Biochemistry & Molecular Biology, MD Anderson Cancer Center
2:05 KEYNOTE PRESENTATION
The Human Epigenome and Cancer
Peter Jones, Ph.D., D.Sc., Director, Norris Comprehensive Cancer Center; Distinguished Professor of Urology, Biochemistry and Molecular Biology, University of Southern California
2:50 Analysis of Epigenetic Alterations to Chromatin during Development
Michelle Barton, Ph.D., Professor, Biochemistry & Molecular Biology, MD Anderson Cancer Center
Chromatin structure, DNA methylation and microRNA’s effect epigenetic regulation of gene expression. We use chromatin immunoprecipitation coupled with high through-put methods of deep sequencing or array hybridization to determine genome-wide regulation of histone modifications and transcription factor interactions. Our major focus is how tumor suppressor p53 recruits modifiers of chromatin structure during regulation of transcription in stem cell differentiation and tissue regeneration.
3:20 Networking Refreshment Break, Exhibit & Poster Viewing
4:00 Aberrant Gene Silencing in Human Cancers by Destabilized Chromatin Boundaries
Beverly Emerson, Ph.D., Professor, Regulatory Biology Lab, Salk Institute for Biological Studies
The p16INK4a tumor suppressor gene is a frequent target of epigenetic inactivation in many human cancers and is considered to be an early event in tumorigenesis. We have identified a chromatin boundary upstream of the p16 gene that is lost when this gene is aberrantly silenced in multiple human cancer cell lines. We show that the multifunctional protein CTCF maintains this boundary and that absence of CTCF binding results in transcriptional silencing and DNA methylation of p16 and other tumor suppressor genes in human breast cancer cell lines. Thus, destabilization of CTCF-dependent chromosomal domains may be a general mechanism to inactivate tumor suppressor genes and initiate tumorigenesis in numerous forms of human cancers.
4:30 Antisense Non-coding RNAs Function as Endogenous Regulators of Transcription in Human Cells
Kevin V. Morris, Ph.D., Assistant Professor, Molecular & Experimental Medicine, Scripps Research Institute
Small RNA targeting of promoters in human cells has been shown to modulate transcriptional gene silencing. While the mechanism involved in transcriptional gene silencing has been shown to require Argonaute 1 (Ago-1), Histone Deactylase 1 (HDAC-1), and DNA methyltransferase 3a (DNMT3a), the endogenous RNA trigger directing these proteins to targeted promoters in human cells had remained unknown. We present evidence here suggesting that long antisense non-coding RNAs function in human cells as effector molecules driving transcriptional gene silencing. This mechanism appears to function via RNA targeted epigenetic changes to homology containing loci.
5:00 Targeted Methylation Sequencing and Applications
Kun Zhang, Ph.D., Assistant Professor, Bioengineering, University of California, San Diego
5:30–7:00 Welcoming Reception in the Exhibit Hall