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Mechanism of Generation of Therapy Related Leukemia in Response to Anti-Topoisomerase II Agents

Author

Listed:
  • Ian G. Cowell

    (Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, Tyne and Wear NE2 4HH, UK)

  • Caroline A. Austin

    (Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, Tyne and Wear NE2 4HH, UK)

Abstract

Type II DNA topoisomerases have the ability to generate a transient DNA double-strand break through which a second duplex can be passed; an activity essential for DNA decatenation and unknotting. Topoisomerase poisons stabilize the normally transient topoisomerase-induced DSBs and are potent and widely used anticancer drugs. However, their use is associated with therapy-related secondary leukemia, often bearing 11q23 translocations involving the MLL gene. We will explain recent discoveries in the fields of topoisomerase biology and transcription that have consequences for our understanding of the etiology of leukemia, especially therapy-related secondary leukemia and describe how these findings may help minimize the occurrence of these neoplasias.

Suggested Citation

  • Ian G. Cowell & Caroline A. Austin, 2012. "Mechanism of Generation of Therapy Related Leukemia in Response to Anti-Topoisomerase II Agents," IJERPH, MDPI, vol. 9(6), pages 1-17, May.
    • Handle: RePEc:gam:jijerp:v:9:y:2012:i:6:p:2075-2091:d:18066
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    References listed on IDEAS

    as
    1. Neelima Mondal & Jeffrey D. Parvin, 2001. "DNA topoisomerase IIα is required for RNA polymerase II transcription on chromatin templates," Nature, Nature, vol. 413(6854), pages 435-438, September.
    2. Andrei V. Krivtsov & David Twomey & Zhaohui Feng & Matthew C. Stubbs & Yingzi Wang & Joerg Faber & Jason E. Levine & Jing Wang & William C. Hahn & D. Gary Gilliland & Todd R. Golub & Scott A. Armstron, 2006. "Transformation from committed progenitor to leukaemia stem cell initiated by MLL–AF9," Nature, Nature, vol. 442(7104), pages 818-822, August.
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