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. Author manuscript; available in PMC: 2009 Nov 15.
Published in final edited form as: Cancer Res. 2008 Nov 15;68(22):9375–9383. doi: 10.1158/0008-5472.CAN-08-2223

Figure 4. Induction of apoptosis in a panel of cell lines with EGFR, RAS and BRAF mutations in response to MEK inhibition.

Figure 4

A. Percent of cells in the sub-G1 population as determined by FACS analysis in the presence or absence of MEK inhibitor (50nM PD0325901 for 72 hours). Error bars represent standard deviation of replicate experiments. MEK inhibition induced a significant increase in sub-G1 fraction in four of five BRAF mutant cell lines. The variable response of H1395 and H1755 cells, which both express the G469ABRAF mutation, suggests that additional genetic heterogeneity within these lines conditions MEK-dependence in NSCLC. B. Immunoblot of activated PARP and caspase-3 in representative EGFR-, KRAS- and BRAF-mutant cell lines in the absence (−) or presence (+) of 50nM PD0325901 for 24 hours.