Completed
PRC2/MYC dysregulation drives evolved BRD4i resistance
Class Central Classrooms beta
YouTube videos curated by Class Central.
Classroom Contents
Functional Genomic Interrogation of Tumor Evolution
Automatically move to the next video in the Classroom when playback concludes
- 1 Intro
- 2 Research Area 1: Context-dependent regulation of survival signaling in cancer
- 3 Research Area 2: Functional tumor evolution
- 4 Vulnerabilities arising during tumor evolution
- 5 Mapping the beneficial and detrimental effects of selinexor
- 6 AKT activation is a beneficial effect of selinexor
- 7 Selinexor-induced P2RY2 upregulation is necessary and sufficient for AKT activation
- 8 P2RY2-driven AKT activation requires p110g, p101, and Ras
- 9 Antagonistic Pleiotropy: Genes that couple sensitivity and resistance
- 10 Systematic analysis of AP
- 11 A PRC2/NSD/MYC AP axis
- 12 PRC2/MYC dysregulation drives evolved BRD4i resistance
- 13 MYC drives BIM-dependent apoptotic priming and BCL-2 inhibitor sensitivity
