It is historically well known that signaling by the PI3K-AKT and MEK1/2-ERK1/2 pathways in a cell type-dependent fashion can collaborate to maintain cell viability. (1)(-) (3) Signaling pathways can also crosstalk with each other wherein one pathway can signal to either enhance or suppress signaling by another. (4) Signaling by the ERK1/2 pathway can also stimulate release of growth factors which can feed back onto tumor cells to re-energize signaling pathways. (5) The studies described by Toulany et al. add to this knowledge base by examining the relationship between PI3K-AKT and MEK1/2-ERK1/2 pathway signaling, EGF receptor signaling, K-RAS function, and tumor cell survival. (6.)
Keywords: EGFR; HNSCC; K-RAS; MAPK/ERK; NSCLC; PI-103; PI3K/Akt; erlotinib.