Cambridge Healthtech Institute’s Fourth Annual
March 5-7, 2012| Hilton San Diego Resort | San Diego, California
Epigenetics refers to the study of heritable changes in gene expression that occur without a change in DNA sequence. Epigenetic mechanisms are multifaceted and complex, and they provide an additional layer of transcriptional control to regulate how genes are expressed. As researchers continue to decipher the roles of DNA, RNA, proteins, and environment in inheritance, the increased understanding of gene regulation and cellular differentiation from embryogenesis to aging will reveal therapeutic interventions as well as diagnostic and prognostic tools for disease.
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Monday, March 5
8:30 am Pre-Conference Short Course Registration
9:00 am-12:00 pm Recommended Pre-Conference Short Courses*
SC1: Epigenetics Toolbox
SC2: Sequencing 101
*Separate registration required.
12:00-2:00 pm Main Conference Registration
2:00 Chairperson's Remarks
Peter Jozsi, Co-Founder and Editor, EpiGenie
» 2:10 Featured Speaker
The Cancer Epigenome
Peter A. Jones, Ph.D., D.Sc., Director of the USC Norris Comprehensive Cancer Center, University of Southern California - Dr. Peter Jones Explains Epigenetics 101 at USC Norris Comprehensive Cancer Center
The epigenome gets profoundly altered in cancer directly participating in carcinogenesis. Recent data from cancer genome mapping studies have uncovered a surprisingly high frequency of mutations in genes which regulate the epigenome. I will discuss the translational opportunities afforded by drugs which can target these changes.
2:45 Epigenetic Effects of Environmental Carcinogens
Ahmad Besaratinia, Ph.D., Associate Research Professor, Cancer Biology, City of Hope, Beckman Research Institute
We have investigated whether epigenetic changes, specifically aberrant DNA methylation and dysregulation of gene expression, alone or in combination with genetic mutations, are involved in the genesis of cancers associated with environmental.
3:20 Selected Poster Presentation: Smyd3 Catalyzes a Novel Methylation Mark and Regulates Cancer Cell Proliferation
Ryan Kruger, Ph.D., Principal Scientist, MMPD Enzymology and Mechanistic Pharmacology, GlaxoSmithKline
3:35 Networking Refreshment Break
4:00 Targeted Therapies Need Targets - Combination Approaches with Epigenetic Therapy to Overcome Resistance to Targeted Therapies in Solid Tumors
Peter Ordentlich, Ph.D., Executive Director, Translational Research, Syndax Pharmaceuticals
Epigenetic processes have been shown to contribute to resistance to targeted therapies often through a loss of expression of the target, or loss of growth dependency on the targeted oncogenic driver. Our goal has been to apply combination strategies with Entinostat, a class 1 histone deacetylase inhibitor, in breast and lung cancer to overcome resistance to hormone therapies and EGFRi respectively. Our approach and results from our phase 2 clinical programs will be presented.
4:35 Metabolism as a Key to HDAC Inhibition
Roderick H. Dashwood, Ph.D., Director, Cancer Chemoprotection Program, Linus Pauling Science Center, Oregon State University
Modulators of histone deacetylase (HDAC) activity have gained interest as both cancer chemopreventive and therapeutic agents. Of the first generation, FDA-approved HDAC inhibitors, Vorinostat represents a "direct acting" compound with structural features suitable for docking into the HDAC pocket, whereas Romidepsin can be considered a pro-drug that undergoes reductive metabolism to generate the active intermediate. It is now evident that other agents, including those in the human diet, can be converted by metabolism to intermediates that affect HDAC activity. Examples will be discussed, including putative endogenous HDAC inhibitors generated by intermediary metabolism (e.g., pyruvate).
5:10 DNA Methylation and Hydroxymethylation in Human Cancer
Srinivasan (Vasan) Yegnasubramanian, M.D., Ph.D., Assistant Professor, Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine
Aberrations in the modifications of cytosine bases in DNA is a universal feature of human cancers. In addition to alterations in the patterns of cytosine methylation, it is now clear that human cancers are often characterized by profound loss of genomic cytosine hydroxymethylation compared to normal tissues. The biological mechanisms behind the acquisition of these alterations in DNA cytosine modifications and the downstream consequences of these alterations in carcinogenesis represent an exciting new frontier in cancer epigenetics.
5:45 Close of Day
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