Figure 5
Figure 5. Tipifarnib treatment provoked RAS inhibition and induced apoptosis of t(6;11)-rearranged cell line. (A) MLL-rearranged cell lines treated with increasing concentrations of chemotherapies (Doxo, Ara-C or VP16; 0.01-10 µM) showed a similar reduction in proliferation, whereas tipifarnib (0.1–100 µM) was specifically reducing ML2 cell proliferation. (B) WB analysis showed p-ERK1/2 reduced levels during increasing tipifarnib treatment in ML2. (C) Histogram represented the ratio between p-ERK and total ERK in ML2: a reduction of p-ERK was visible after tipifarnib treatment. (D) WB analysis showed BCL2-like 11 (apoptosis facilitator) (BIM) and PARP cleavage increased after tipifarnib treatment in ML2. (E) WB analysis showed mechanistic target of rapamycin (serine/threonine kinase) (mTOR) and p70S6K phosphorylated and total protein after tipifarnib treatment in ML2 and THP-1.

Tipifarnib treatment provoked RAS inhibition and induced apoptosis of t(6;11)-rearranged cell line. (A) MLL-rearranged cell lines treated with increasing concentrations of chemotherapies (Doxo, Ara-C or VP16; 0.01-10 µM) showed a similar reduction in proliferation, whereas tipifarnib (0.1–100 µM) was specifically reducing ML2 cell proliferation. (B) WB analysis showed p-ERK1/2 reduced levels during increasing tipifarnib treatment in ML2. (C) Histogram represented the ratio between p-ERK and total ERK in ML2: a reduction of p-ERK was visible after tipifarnib treatment. (D) WB analysis showed BCL2-like 11 (apoptosis facilitator) (BIM) and PARP cleavage increased after tipifarnib treatment in ML2. (E) WB analysis showed mechanistic target of rapamycin (serine/threonine kinase) (mTOR) and p70S6K phosphorylated and total protein after tipifarnib treatment in ML2 and THP-1.

Close Modal

or Create an Account

Close Modal
Close Modal