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AraC resistance in TP53 m ut AML requires the mevalonate pathway byproduct, GGPP m ut To determine the specific mevalonate pathway byproducts necessary for mitochondria-dependent chemoresistance, we performed rescue experiments in the representative TP53 mut AML clone, M14-Mut1, treated with a rescue agent and rosuvastatin for 48 h with AraC added for the last 24 h (Schema summarizing targets in Fig

The frequencies presented, therefore, represent the proportion of the 3525 individuals exposed to clomipramine who experienced an event of the type cited on at least one occasion while receiving clomipramine