A mathematical model shows that mutations that recur even modestly among cancer patients are cancer driving nucleotides that can be exhaustively identified to serve as targets of cancer therapy.
Structure-based designed chalcone and pyrazoline derivatives inhibited the ELF3-MED23 protein-protein interaction, leading to HER2 downregulation and retardation of tumor growth in HER2-positive gastric cancer.
The local PI(4,5)P2 nanodomain promotes the dimerization and activation of EGFR in the plasma membrane, whereas activated EGFR dissolves the nanodomain structure of PI(4,5)P2 through PLCγ.
