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Ruxolitinib treatment reduces monocytic superoxide radical formation without affecting hydrogen peroxide formation or systemic oxidative nucleoside damage in myelofibrosis

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  1. Markers of HPA-axis activity and nucleic acid damage from oxidation after electroconvulsive stimulations in rats

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  2. Oxidatively generated modifications to nucleic acids in vivo: Measurement in urine and plasma

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  3. The Effect of Different Training Intensities on Oxidatively Generated Modifications of Nucleic Acids: A Randomized, Controlled Trial

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The role of excess reactive oxygen species (ROS) with consequent DNA/RNA damage is now recognized as a hallmark of cancer. In JAK2V617F mutated myeloproliferative neoplasms, ROS have been suggested to be important factors in disease initiation and progression. Ruxolitinib is the most widely used drug for myelofibrosis, because it improves symptom-score. However, both the anti-clonal potential and improvement in overall survival are limited. We investigated the impact of ruxolitinib on formation of superoxide radical and hydrogen peroxide by monocytes in sequentially acquired blood samples from patients with myelofibrosis. We also investigated the impact on RNA and DNA damage by measuring urinary excretion of 8-oxo-Guo and 8-oxo-d-Guo. The formation of superoxide by monocytes was reduced significantly during ruxolitinib therapy, but no impact on the formation of hydrogen peroxide by monocytes or the systemic amount of oxidatively damaged RNA or DNA could be demonstrated. We conclude that ruxolitinib holds little anti-oxidative potential.

Original languageEnglish
JournalLeukemia and Lymphoma
Issue number10
Pages (from-to)2549-2557
Number of pages9
Publication statusPublished - 2019

    Research areas

  • DNA damage, hydrogen peroxide, myelofibrosis, Reactive oxygen species, ruxolitinib, superoxide radical

ID: 56643066