New research has found a possible way of determining which patients with acute myeloid leukaemia might respond best to cytarabine-based therapy.
This well-established treatment is a form of chemotherapy, often given by continuous intravenous infusion. It kills cancer cells by interfering with the synthesis of DNA.
But Dr Oliver Keppler, of the University of Frankfurt, Germany, and colleagues say that, despite a high rate of initial remissions, a substantial fraction of patients relapse and acquire resistance to cytarabine. Patients in this group, particularly older patients, have a poor prognosis.
The team point out that mutations in the SAMHD1 gene, have been linked with cancers including some forms of leukaemia. Enhancing the action of SAMHD1 increases the efficacy of certain HIV drugs, so the team tested whether it could have a similar effect on cytarabine-based therapy for leukaemia.
In tests on mice and on cells from patients, the experts found that SAMHD1 does indeed boost cytarabine cytotoxicity in acute myeloid leukaemia cells. It does so by removing the phosphate residues from the active form of cytarabine and reversing it into its inactive state.
"The toxicity of cytarabine against acute myeloid leukaemia cells correlates with the expression of the cellular enzyme SAMHD1, which enables to accurately predict the sensitivity of acute myeloid leukaemia cells to cytarabine," they wrote in Nature Medicine.
"These results identify SAMHD1 as a potential clinical biomarker for the stratification of patients with acute myeloid leukaemia who might best respond to cytarabine-based therapy, and as a target for treating cytarabine-resistant acute myeloid leukaemia," they add.
Source: Schneider, C. et al. SAMHD1 is a biomarker for cytarabine response and a therapeutic target in acute myeloid leukemia. Nature Medicine 19 December 2016; doi: 10.1038/nm.4255
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