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Targeting Cancer Pathways: Tumor Metabolism and Proliferation

Participating Experts: M. Celeste Simon, PhD (U. Penn) and Nissim Hay, PhD (U. Illinois). ⬇️ Expand “Show More” to view abstract and table of contents View Cellular Metabolism signaling pathway diagrams: https://cst-science.com/hb1cn5 This webinar explores how cancer cells are able to reprogram their metabolic pathways to enable energy production under conditions that are disabling to most normal cells. Of particular interest are how tumor-specific metabolic changes promote oncogenic progression and how these changes can be exploited to develop more effective treatment options. Topics covered include: • The major metabolic changes in tumor tissue; • How specific metabolic pathways can be targeted during therapeutic interventions; • The role of autophagy and cell death in tumor survival and progression Table of Contents 0:23 Welcome and overview 2:51 Celeste Simon speaker profile 3:35 Hypoxia, metabolism, and tumor progression 4:05 Limited oxygen availability in solid tumors 5:20 Tumor blood vessel phenotypes 8:32 Regulation of hypoxia-inducible factor (HIF) stability and activity 9:53 Metabolic pathways active in proliferating cells 11:18 ccRCC, predominant subtype of kidney cancer 12:49 Metabolic profiling of ccRCC tumor and normal kidney 14:40 central carbon metabolism 16:05 FBP1 inhibits HIF in the nucleus 17:53 FBP1 associates with HIF-1α and HIF-1β 18:28 Conclusion 21:34 Nissim Hay speaker profile 22:23 Exploiting glucose metabolism in cancer cells for cancer therapy 22:41 Selective detection of cancer in vivo by exploiting high rate of glycolysis 24:34 Hexokinases catalyze the first committed step in glucose metabolism 26:14 Expression of hexokinase 1/2 in embryonic and adult tissues 28:34 K-ras driven NSCLC in mice 29:57 Hexokinase 2 deletion in K-ras mouse lung tumors decreased mortality and attenuates tumor burden 31:10 Hexokinase 2 expression in NSCLC correlated with patient survival 32:33 Hexokinase 2 deletion prolongs tumor onset and inhibits incidence of ErbB2/Neu driven mouse mammary tumors 35:05 K-ras-LA2 mouse model of lung cancer 37:34 Isoform switch in liver tumors 38:49 Hexokinase 2 is highly expressed in human HCC regardless of cause 39:49 HK2 activity is required for proliferation and oncogenesis of HCC cells 41:43 Delection of HK2 in Pten / prostate neoplasia inhibits proliferation and induces apotosis 42:48 Summary 44:25 Questions and answers About CST®: Cell Signaling Technology (CST) is a private, family-owned company, founded by scientists and dedicated to providing high-quality research tools to the biomedical research community. Our employees operate worldwide from our U.S. headquarters in Massachusetts, and our offices in the Netherlands, China, and Japan. https://cellsignal.com/about All trademarks are the property of their respective owners. For the most up-to-date trademark information, please visit https://www.cellsignal.com/trademarks #Antibody #CSTWebinar