Figure 7
Figure 7. Primary relapse ALL samples demonstrate increased sensitivity to prednisolone upon trametinib inhibition and increased pERK levels compared to diagnosis samples. (A) Phospho flow cytometry analysis of 7 matched diagnosis-relapse primary samples for levels of pERK. A statistically significant increase (P < .0025) in phosphorylated ERK at relapse compared to diagnosis was found. (B) Absolute blast count in mice engrafted with a matched diagnosis-relapse pair treated with control vehicle or trametinib. (C) Five primary diagnosis-relapse matched pairs were treated ex vivo with trametinib, prednisolone, or combination of trametinib and prednisolone for 48 hours. The cells were stained for activated caspase 3 as a measure of cell viability by phospho flow cytometry. (D) Splenic blast count in mice engrafted with relapse samples treated with vehicle (Untx), trametinib (Tram), dexamethasone (Dex), or a combination (Combo) of trametinib and dexamethasone.

Primary relapse ALL samples demonstrate increased sensitivity to prednisolone upon trametinib inhibition and increased pERK levels compared to diagnosis samples. (A) Phospho flow cytometry analysis of 7 matched diagnosis-relapse primary samples for levels of pERK. A statistically significant increase (P < .0025) in phosphorylated ERK at relapse compared to diagnosis was found. (B) Absolute blast count in mice engrafted with a matched diagnosis-relapse pair treated with control vehicle or trametinib. (C) Five primary diagnosis-relapse matched pairs were treated ex vivo with trametinib, prednisolone, or combination of trametinib and prednisolone for 48 hours. The cells were stained for activated caspase 3 as a measure of cell viability by phospho flow cytometry. (D) Splenic blast count in mice engrafted with relapse samples treated with vehicle (Untx), trametinib (Tram), dexamethasone (Dex), or a combination (Combo) of trametinib and dexamethasone.

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