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癌細胞がグルコース代謝を変化させるという事実によって、医薬品業界では、腫瘍を標的とする新たな方法の探究に新たな関心が寄せられています。癌細胞におけるグルコース消費増加を反転させることは重要なステップであり、治療薬開発の大きな可能性をもっています。この会議は、癌細胞の代謝の変え方に関する現在の戦略と、それに伴う新たな分子薬剤標的開発のための機会に焦点が当てられています。 11月2日（水） 7:00 am Conference Registration and Morning Coffee 8:30 Chairperson’s Opening Remarks 新規の標的 8:40 Malic Enzyme 2 (ME2) as a Novel Cancer Metabolic Target Vikas Sukhatme, Professor, Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School We have discovered that ME2 is widely overexpressed in a number of tumor types. Its inhibition can decrease tumor growth and induce differentiation in vitro and in vivo. 9:10 Targeting Atypical Glucose Transporter Regulation in Multiple Myeloma with HIV Protease Inhibitors Mala Shanmugam, Ph.D., Research Assistant Professor , Robert H.Lurie Comprehensive Cancer Center, Northwestern University Tumor cells, including the fatal B cell malignancy multiple myeloma, consume surprisingly high amounts of glucose. While elevated glucose utilization forms the basis for clinical imaging of various cancers, we are not yet able to target glucose utilization for therapy. We have identified a subset of glucose transporters (GLUTs) that are uniquely regulated in myeloma including the insulin-responsive glucose transporter GLUT4, providing targeting opportunities selective to these tumor cells. In addition we have identified an FDA approved HIV protease inhibitor that has an off-target effect on GLUT4, warranting repositioning of this class of compounds for the treatment of GLUT4-dependent cancers. Our studies range from target identification, in vitro cell line validation and ex vivo pre-clinical studies in myeloma patient samples providing novel approaches to treat this incurable cancer. 9:40 Speaker to be Announced 10:10 Grand Opening Coffee Break in the Exhibit Hall with Poster Viewing
• 解糖およびワークブルグ効果 10:40 Talk Title to be Announced Kate Yen, Ph.D., Associate Director, Biology, Agios Pharmaceuticals, Inc. 11:10 Sponsored Presentations (Opportunities Available) 11:40 Targeting the Warburg Effect by Synthetic Lethality Ray Tabibiazar, M.D., CEO, Ruga Corporation Paul Pearson, Ph.D., VP, Pre-Clinical Development, Ruga Corporation Identifying new molecular targeted therapies that specifically kill tumor cells while sparing normal tissue is the next major challenge of cancer research. We describe here strategies to target the Warburg Effect in a genetically defined patient population by utilizing synthetic lethality. 12:10 pm Interfering with Cancer Cell Signaling Speaker to be Announced 12:40 Luncheon Presentation (Sponsorship Opportunity Available) or Lunch on Your Own 2:20 Chairperson’s Remarks 2:25 Conserved Features of Cancer Cells Define their Sensitivity of HAMLET-Induced Death; C-Myc and the Warburg Effect Petter Storm, Scientist, Laboratory Medicine, Microbiology, Immunology and Glycobiology (MIG), Lund University HAMLET is the first member of a new family of tumoricidal protein-lipid complexes, and has shown great promise as a human drug candidate, with therapeutic efficacy against skin papillomas and rapid topical effects on human bladder cancers. The results of our research identify HAMLET as a novel anti-cancer agent that exploits unifying features of cancer cells for its activity, including c-Myc and the shift in glycolysis known as the ’’Warburg effect’’. 2:55 Talk Title to be Announced Charles Wenner, Ph.D., Department of Cell and Molecular Biology, Roswell Park Cancer Institute 3:25 Networking Refreshment Break in the Exhibit Hall with Poster Viewing 4:05 Development of Chemical Probes to Study Cancer Metabolic Reprogramming Sergey A. Kozmin, Ph.D., Associate Professor, Chemistry, University of Chicago Understanding of the nature of reprogrammed energy metabolism in cancer cells is of significant current interest. We will describe the development of an arsenal of new small-molecule probes to study altered energy metabolism in cancer. This study is aimed at identifying the underlying reasons for major alterations in energy producing pathways employed by rapidly proliferating cells and testing the possibility of targeting such cells in vitro and in vivo. 4:35 Potent Anti-Cancer Lipoate Analogs Selectively Attack Tumor Cell Mitochondrial Metabolism Paul Bingham, Ph.D., Vice President, Research, Cornerstone Pharmaceuticals Among the enzymes whose regulation is reprogrammed in many tumor cells is the pyruvate dehydrogenase complex (PDH). The lipoate moieties of PDH serve both catalytic and regulatory function. Non-redox active lipoate analogs apparently attack cancers-specific elements of this lipoate-sensitive regulatory apparatus, causing cancer cell death in cell culture and in human tumor xenograft models. 5:05 Interactive Breakout Discussion Groups 6:15 – 7:15 Welcoming Reception in the Exhibit Hall with Poster Viewing
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