Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital

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

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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

    Publikation: Bidrag til tidsskriftReviewForskningpeer review

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

    Publikation: Bidrag til tidsskriftKonferenceabstrakt i tidsskriftForskningpeer review

Vis graf over relationer

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.

TidsskriftLeukemia and Lymphoma
Udgave nummer10
Sider (fra-til)2549-2557
Antal sider9
StatusUdgivet - 2019

ID: 56643066