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Results: Cytarabine blunted cholesterol biosynthesisand induced CD36-mRNA expression under 1% and 21% O2. ICCLs were significantly higher in Cytarabine treated AML cells compared to untreated controls. Treatment with Rosuvastatin significantly inhibited growth of M14, THP1, OCI-AML3 as well as AML PCs (n=3). Further, Rosuvastatin lowered ICCLs and conferred pro-apopotic and growth inhibitory effects against M14 and THP-1 cells. Growth inhibition was enhanced when Rosuvastatin was combined with Cytarabine, yielding additive to synergistic effects. Similar effects were observed in AML PCs (n=10) where Rosuvastatin combined with Cytarabine demonstrated strong synergy.

Genoproteomic analysis of leukemic cell response to Cytarabine reveals synergistic opportunities centered on cholesterol metabolism