Figure 6
Figure 6. Tipifarnib treatment provoked RAS inhibition and induces apoptosis of t(6;11)-rearranged primary cells. (A) The t(6;11) primary cell cultures treated with increasing concentration of tipifarnib showed an accentuated induction of apoptosis (percentage of Annexin V/propidium iodide-positive cells), especially with increasing drug concentrations with respect to primary AML cultures with different MLL-translocation. (B) (Left) WB analysis showed p-ERK1/2 reduced levels during increasingly tipifarnib treatment. LC3 and p62 documented autophagy induction at low tipifarnib doses, whereas PARP cleavage confirmed apoptosis when higher doses of tipifarnib was used. Anti-ACTIN was used as positive control for protein amount. (Right) Histogram represented the ratio between p-ERK and total ERK: a reduction of p-ERK was visible after tipifarnib treatment at any concentration.

Tipifarnib treatment provoked RAS inhibition and induces apoptosis of t(6;11)-rearranged primary cells. (A) The t(6;11) primary cell cultures treated with increasing concentration of tipifarnib showed an accentuated induction of apoptosis (percentage of Annexin V/propidium iodide-positive cells), especially with increasing drug concentrations with respect to primary AML cultures with different MLL-translocation. (B) (Left) WB analysis showed p-ERK1/2 reduced levels during increasingly tipifarnib treatment. LC3 and p62 documented autophagy induction at low tipifarnib doses, whereas PARP cleavage confirmed apoptosis when higher doses of tipifarnib was used. Anti-ACTIN was used as positive control for protein amount. (Right) Histogram represented the ratio between p-ERK and total ERK: a reduction of p-ERK was visible after tipifarnib treatment at any concentration.

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