text_1: Combining phosphatidylinositide 3-kinase and MEK 1/2 inhibitors is effective at treating KRAS mutant tumors.
text_2: Mutant PI3K (PIK3CA) and loss of PTEN activity were sufficient, but not necessary, as predictors of sensitivity to the antitumor activity of the PI3K inhibitor PX-866 in the presence of wild-type Ras, whereas mutant oncogenic Ras was a dominant determinant of resistance, even in tumors with coexisting mutations in PIK3CA.