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Common themes in the pathogenesis of acute myeloid leukemia

Oncogene volume 20, pages 5680–5694 (2001)Cite this article

Abstract

The pathogenesis of acute myeloid leukemia is associated with the appearance of oncogenic fusion proteins generated as a consequence of specific chromosome translocations. Of the two components of each fusion protein, one is generally a transcription factor, whereas the other partner is more variable in function, but often involved in the control of cell survival and apoptosis. As a consequence, AML-associated fusion proteins function as aberrant transcriptional regulators that interfere with the process of myeloid differentiation, determine a stage-specific arrest of maturation and enhance cell survival in a cell-type specific manner. The abnormal regulation of transcriptional networks occurs through common mechanisms that include recruitment of aberrant co-repressor complexes, alterations in chromatin remodeling, and disruption of specific subnuclear compartments. The identification and analysis of common and specific target genes regulated by AML fusion proteins will be of fundamental importance for the full understanding of acute myeloid leukemogenesis and for the implementation of disease-specific drug design.

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Acknowledgements

The authors thank Dr Lucilla Luzi for the graphics included in this review.

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Authors and Affiliations

  1. Department of Experimental Oncology, European Institute of Oncology, 20141 Milan, Italy

    Myriam Alcalay, Natalia Meani, Ferdinando Chiaradonna, Saverio Minucci & Pier Giuseppe Pelicci

  2. Università degli Studi di Perugia, Policlinico Monteluce, 06100 Perugia, Italy

    Annette Orleth, Carla Sebastiani, Cristina Casciari, Maria Teresa Sciurpi, Vania Gelmetti, Daniela Riganelli & Marta Fagioli

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  1. Myriam Alcalay
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  2. Annette Orleth
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  3. Carla Sebastiani
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Correspondence to Myriam Alcalay.

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Alcalay, M., Orleth, A., Sebastiani, C. et al. Common themes in the pathogenesis of acute myeloid leukemia. Oncogene 20, 5680–5694 (2001). https://doi.org/10.1038/sj.onc.1204642

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