This effect of dual inhibition in general did not reach statistical significance for additivity nor being synergistic in either cluster ( Figures 2E and F ), although at the highest concentrations (5 μ M CI-1040 with 10 n M rapamycin) in the LKB1/KRAS mutant cluster, the data were consistent with an additive model.
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LKB1/KRAS mutant lung cancers constitute a genetic subset of NSCLC with increased sensitivity to MAPK and mTOR signalling inhibition.
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