BioProject

We found that hepatic injury induced by PTEN loss establishes a selection pressure for tumorinitiating cells (TICs) to proliferate and form mixed lineage tumors. More...

We found that hepatic injury induced by PTEN loss establishes a selection pressure for tumorinitiating cells (TICs) to proliferate and form mixed lineage tumors. The Pten null mice demonstrate escalating levels of hepatic injury prior to proliferation of hepatic progenitors. Attenuation of hepatic injury by deleting Akt2 reduces progenitor cell proliferation and delays tumor development. Treatment of double mutant mice with 3,5-dietoxycarbonyl-1,4 dihydrocollidine (DDC) shows that the primary effect of AKT2 loss is attenuation of hepatic injury and not inhibition of progenitor cell proliferation in response to injury. Overall design: Pten/Akt2 double mutant (PtenloxP/loxP; Akt2-/-; Alb-Cre+) (Dm) were generated by crossing the PtenloxP/loxP; Alb-Cre+ (Pm) with the Akt2-/- mice [19]. Control animals are PtenloxP/loxP; Albumin (Alb)-Cre-. Less...