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. 2018 Aug;32(8):1818-1822.
doi: 10.1038/s41375-018-0032-1. Epub 2018 Apr 7.

Proteomic and genomic integration identifies kinase and differentiation determinants of kinase inhibitor sensitivity in leukemia cells

Pedro Casado  1 , Edmund H Wilkes  1 , Farideh Miraki-Moud  2 , Marym Mohammad Hadi  1 , Ana Rio-Machin  3 , Vinothini Rajeeve  1 , Rebecca Pike  4 , Sameena Iqbal  5 , Santiago Marfa  1 , Nicholas Lea  6 , Steven Best  6 , John Gribben  2 , Jude Fitzgibbon  3 , Pedro R Cutillas  7
Affiliations

Proteomic and genomic integration identifies kinase and differentiation determinants of kinase inhibitor sensitivity in leukemia cells

Pedro Casado et al. Leukemia. 2018 Aug.
No abstract available

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Association of differentiation, kinase activity, and sensitivity to kinase inhibitors in primary AML. a Sensitivity to MEKi as a function of FAB group. b CD expression across 30 cases and estimation of individual kinase activities in CDs+ and CDs− groups. c Sensitivity to kinase inhibitors as a function of CD pattern expression. Significance was assessed by Mann–Whitney test in a, c and with a z-test in b
Fig. 2
Fig. 2
Integration of genomic, phosphoproteomics, and mass cytometry data to rationalize kinase inhibitors sensitivity. a Viability of AML cells within the indicated genotype/phenotype groups after treatment with MEKi. b Sensitivity of NRAS/BRAF/CDs+ positive cells to MEKi as a function of the indicated factors. c FLT3/PKCi sensitivity of AML cells with the indicated phenotype/genotype. Phosphorylations are denoted as (hi) and (lo) based on a greater or lower phosphorylation than the median across all cases. Significance was assessed by Mann–Whitney test
See this image and copyright information in PMC

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