236 BMI1 PROMOTES THE CARCINOGENESIS OF RAT HEPATIC PROGENITOR CELLS

LDG treated group.Histological evaluation on normal organs of increased pERK level in GE/sorafenib treated mouse showed some inflammatory change, suggesting pERK activation by LDG may cause unexpected toxicity in normal cells.Conclusions: Combinational GE and sorafenib showed synergistic effect on antitumoral activity of sorafenib via GE mediated pERK stimulation.However, concomitant use of both sorafenib and GE may induce a potential toxicity of sorafenib due to pERK stimulation in normal organs.Previously pERK level has been provided as potential predictive marker for sorafenib.This is the first report suggesting that the antitumoral activity of sorafenib can be sensitized by pharmacological modulation of pERK level.