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Wilms' tumor 1 mutation accumulated during therapy in acute myeloid leukemia: biological and clinical implications

Leukemia volume 20, pages 2051–2054 (2006)Cite this article

Molecular biology is a powerful tool for investigating acute myeloid leukemia (AML). Given that concerted efforts have documented the reliability and clinical utility of the real-time quantitative polymerase chain reaction (RQ-PCR) for detecting fusion transcripts in AML,1 it is not surprising that similar assays have been sought for in the sizeable fraction of AML cases without balanced translocations. The Wilms' tumor gene 1 (WT1) has received close attention in this respect. Initially described in childhood genitourinary cancers, the gene has subsequently been shown to be overexpressed in a number of different cancers. Although its exact function in the evolvement of a malignant clone is still a matter of debate, its role as an minimal residual disease (MRD) target in myelodysplastic syndrome and AML is now amply documented.2, 3 Indeed, recent data from our laboratory suggest that the assay is able to predict relapse months ahead of morphological relapse.2, 4

In de novo AML relapses are often thought to emerge from exactly the same clone as at diagnosis. This is in contrast to the situation in, for example, pre-B acute lymphoid leukemia, where IgH gene rearrangements have disclosed clonal instability.

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Acknowledgements

This work was supported by grants from the Danish Cancer Society, the Danish Research Agency, and the Karen Elise Jensen Foundation. We thank Mette Østergaard for helpful suggestions, Gitte Biller for excellent technical assistance, and David Grimwade, Guy's King's and St Thomas' School of Medicine, for careful review of this paper.

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Authors and Affiliations

  1. Department of Hematology, Aarhus University Hospital, Aarhus, Denmark

    C G Nyvold, J Stentoft, K Brændstrup, D Melsvik, C Juhl-Christensen & P Hokland

  2. Department of Medical Biochemistry, Aarhus University, Aarhus, Denmark

    S K Moestrup

  3. Department of Pediatrics, Skejby Hospital, Aarhus, Denmark

    H Hasle

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  1. C G Nyvold
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Correspondence to P Hokland.

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Nyvold, C., Stentoft, J., Brændstrup, K. et al. Wilms' tumor 1 mutation accumulated during therapy in acute myeloid leukemia: biological and clinical implications. Leukemia 20, 2051–2054 (2006). https://doi.org/10.1038/sj.leu.2404389

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