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Altered expression of tumor suppressor PHF20 in myeloproliferative neoplasms

Leukemia volume 28, pages 1762–1764 (2014)Cite this article

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Myeloproliferative neoplasms (MPN) arise from somatic mutations at the level of the hematopoietic stem cell, which result in abnormal expansion of the myeloid compartment. Clonal myelopoiesis in MPN is accompanied by genomic instability, which promotes the accumulation of biologically more aggressive subclones that ultimately undergo leukemic transformation. The molecular or biological mechanisms behind clonal evolution in MPN and other myeloid malignancies are complex and cumulative.1

We recently reported the identification of several novel DNA alterations in primary myelofibrosis (PMF), a subtype of MPN, using high-resolution mate-pair sequencing (HRMPS).2 In one patient with del(20q), HRMPS revealed breakpoints at 20q11.22 at position 34383499 and 20q13.2 at position 49891766. One of these breakpoints involved the gene plant homeodomain finger 20 (PHF20), resulting in monoallelic genomic loss distal to exon 1.

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Authors and Affiliations

  1. Mayo College of Medicine, Mayo Clinic, Rochester, MN, USA

    T L Lasho

  2. Division of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA

    A Pardanani & A Tefferi

  3. Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA

    D I Smith

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  1. T L Lasho
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  2. A Pardanani
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  3. A Tefferi
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  4. D I Smith
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Correspondence to D I Smith.

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Lasho, T., Pardanani, A., Tefferi, A. et al. Altered expression of tumor suppressor PHF20 in myeloproliferative neoplasms. Leukemia 28, 1762–1764 (2014). https://doi.org/10.1038/leu.2014.117

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