Explore a 25-minute webinar on functional genomic interrogation of tumor evolution presented by Dr. Kris C. Wood, Associate Professor at Duke University. Delve into two key aspects of cancer biology: context-dependent regulation of survival signaling and functional tumor evolution. Examine vulnerabilities arising during tumor evolution, focusing on the effects of selinexor and AKT activation. Investigate the role of P2RY2 upregulation in AKT activation and its dependence on p110g, p101, and Ras. Analyze the concept of antagonistic pleiotropy in cancer genes and the systematic analysis of the APA PRC2/NSD/MYC AP axis. Discover how PRC2/MYC dysregulation drives evolved BRD4i resistance and how MYC influences BIM-dependent apoptotic priming and BCL-2 inhibitor sensitivity. Gain insights into cutting-edge cancer research and potential therapeutic approaches.
Functional Genomic Interrogation of Tumor Evolution
Overview
Syllabus
Intro
Research Area 1: Context-dependent regulation of survival signaling in cancer
Research Area 2: Functional tumor evolution
Vulnerabilities arising during tumor evolution
Mapping the beneficial and detrimental effects of selinexor
AKT activation is a beneficial effect of selinexor
Selinexor-induced P2RY2 upregulation is necessary and sufficient for AKT activation
P2RY2-driven AKT activation requires p110g, p101, and Ras
Antagonistic Pleiotropy: Genes that couple sensitivity and resistance
Systematic analysis of AP
A PRC2/NSD/MYC AP axis
PRC2/MYC dysregulation drives evolved BRD4i resistance
MYC drives BIM-dependent apoptotic priming and BCL-2 inhibitor sensitivity
Taught by
Labroots
