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MLL methylation is not likely a common mechanism for therapy-related AML

Leukemia volume 19, pages 1291–1292 (2005)Cite this article

TO THE EDITOR

Some observations support the hypothesis that hypomethylation is associated with increased DNA recombination, chromosomal aberrations, mitotic dysfunction and translocations,1, 2 and an increased tumor formation rate.3, 4 The MLL gene is often disrupted by chromosomal translocation in infant ALL and AML, in de novo AML, and in therapy-related myeloid leukemia (t-ML) following topoisomerase II inhibitors, such as etoposide. MLL seems to be particularly prone to cleavage following exposure to apoptotic stimuli, and it has been suggested that MLL transcription is required for its rearrangement. We investigated whether there was interindividual variability in methylation status of the MLL gene itself, as such epigenetic variability could predispose to leukemia or t-ML. We used DNA from blasts from nine patients (five diagnostic ALL and four t-ML, all carrying an MLL rearrangement), and from two leukemia cell lines (CEM and Nalm-6). As controls, we also screened DNA from lymphoblastoid cell lines from the DNA Polymorphism Discovery Resource subset (n=8, Coriell Institute), which are representative of human genetic variability.5

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Authors and Affiliations

  1. Department of Pharmaceutical Sciences, St Jude Children's Research Hospital, The University of Tennessee, Memphis, TN, USA

    A Bogni & M V Relling

  2. Department of Hematology/Oncology St Jude Children's Research Hospital, The University of Tennessee, Memphis, TN, USA

    C-H Pui

  3. College of Medicine, The University of Tennessee, Memphis, TN, USA

    C-H Pui & M V Relling

  4. College of Pharmacy, The University of Tennessee, Memphis, TN, USA

    M V Relling

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  1. A Bogni
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  2. C-H Pui
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  3. M V Relling
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Correspondence to M V Relling.

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Bogni, A., Pui, CH. & Relling, M. MLL methylation is not likely a common mechanism for therapy-related AML. Leukemia 19, 1291–1292 (2005). https://doi.org/10.1038/sj.leu.2403768

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  • DOI: https://doi.org/10.1038/sj.leu.2403768

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