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Bone Marrow Clonogenic Myeloid Progenitors from NPM1-Mutated AML Patients Do Not Harbor the NPM1 Mutation: Implication for the Cell-Of-Origin of NPM1+ AML
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Nucleophosmin 1 Mutations in Acute Myeloid Leukemia

1
Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
2
Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
*
Author to whom correspondence should be addressed.
Genes 2020, 11(6), 649; https://doi.org/10.3390/genes11060649
Received: 19 May 2020 / Revised: 6 June 2020 / Accepted: 9 June 2020 / Published: 12 June 2020
(This article belongs to the Special Issue Genetics and Genomics of Acute Myeloid Leukemia)
Nucleophosmin (NPM1) is a ubiquitously expressed nucleolar protein involved in ribosome biogenesis, the maintenance of genomic integrity and the regulation of the ARF-p53 tumor-suppressor pathway among multiple other functions. Mutations in the corresponding gene cause a cytoplasmic dislocation of the NPM1 protein. These mutations are unique to acute myeloid leukemia (AML), a disease characterized by clonal expansion, impaired differentiation and the proliferation of myeloid cells in the bone marrow. Despite our improved understanding of NPM1 mutations and their consequences, the underlying leukemia pathogenesis is still unclear. Recent studies that focused on dysregulated gene expression in AML with mutated NPM1 have shed more light into these mechanisms. In this article, we review the current evidence on normal functions of NPM1 and aberrant functioning in AML, and highlight investigational strategies targeting these mutations. View Full-Text
Keywords: AML; nucleophosmin (NPM1); gene expression; targeted therapies AML; nucleophosmin (NPM1); gene expression; targeted therapies
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MDPI and ACS Style

Zarka, J.; Short, N.J.; Kanagal-Shamanna, R.; Issa, G.C. Nucleophosmin 1 Mutations in Acute Myeloid Leukemia. Genes 2020, 11, 649.

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