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. Author manuscript; available in PMC: 2019 Jul 1.
Published in final edited form as: Mol Cancer Ther. 2018 Apr 13;17(7):1526–1539. doi: 10.1158/1535-7163.MCT-17-0464

Figure 4. NCI-H2077-R cells have a secondary NRAS mutation, rendering them more sensitive to inhibition of the MAPK pathway.

Figure 4

A) NCI-H2077 parental cells are sensitive to BGJ398. Treatment with increasing concentration of BGJ398 over time lead to the emergence of a resistant clone (H2077-R), which is insensitive to BGJ398.

B) Illumina sequencing analysis of 504 cancer and cancer-related genes revealed a canonical NRAS Q61R mutation in H2077-R cells (indicated by the red arrow over the sequencing reads). A schematic of the altered DNA and protein sequences is shown.

C) Cell viability assays of NCI-H2077 and H2077-R treated with BGJ398, trametinib (MEK inhibitor) or combination treatment, as indicated. Combination of non-lethal concentration of BGJ398 and increasing concentration of trametinib preferentially inhibited NCI-H2077-R cells, with modest additional effect on NCI-H2077 cells compared to BGJ398 treatment alone.