Molecular Inhibitors of Growth Signals

Abstract

Signal transduction associated with growth factor receptors typically mediates the activation of cell cycle promoting gene products or the inactivation of cell cycle checkpoints. These signals are frequently transduced through G-Protein pathways, kinase receptor pathways, or nuclear receptor pathways (Fig. 4.1), are dependent on proto-oncogenic transcription factors, and lead to the expression of Cyclins and Cyclin-Dependent Kinases (CDKs), which are drivers of the cell cycle (Fig. 4.2). Physiologically, growth signals are transient and entirely depend on the engagement of a growth factor receptor by its cognate ligand. Upon termination of this interaction, the growth signal ceases. Gain-of-function mutations in cancer keep the growth signal active, regardless of the presence of the transient growth factor-receptor interaction. Such deregulated signaling cascades are appropriate drug targets in the treatment of cancer.