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Kaufmann, Kai B.; Gründer, Albert; Hadlich, Tobias; Wehrle, Julius; Gothwal, Monika; Bogeska, Ruzhica; Seeger, Thalia S.; Kayser, Sarah; Pham, Kien-Binh; Jutzi, Jonas S.; Ganzenmüller, Lucas; Steinemann, Doris; Schlegelberger, Brigitte; Wagner, Julia M.; Jung, Manfred; Will, Britta; Steidl, Ulrich; Aumann, Konrad; Werner, Martin; Günther, Thomas; Schüle, Roland; Rambaldi, Alessandro; Pahl, Heike L.

A novel murine model of myeloproliferative disorders generated by overexpression of the transcription factor NF-E2

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  • Medientyp: E-Artikel
  • Titel: A novel murine model of myeloproliferative disorders generated by overexpression of the transcription factor NF-E2
  • Beteiligte: Kaufmann, Kai B.; Gründer, Albert; Hadlich, Tobias; Wehrle, Julius; Gothwal, Monika; Bogeska, Ruzhica; Seeger, Thalia S.; Kayser, Sarah; Pham, Kien-Binh; Jutzi, Jonas S.; Ganzenmüller, Lucas; Steinemann, Doris; Schlegelberger, Brigitte; Wagner, Julia M.; Jung, Manfred; Will, Britta; Steidl, Ulrich; Aumann, Konrad; Werner, Martin; Günther, Thomas; Schüle, Roland; Rambaldi, Alessandro; Pahl, Heike L.
  • Erschienen: Rockefeller University Press, 2012
  • Erschienen in: Journal of Experimental Medicine
  • Sprache: Englisch
  • DOI: 10.1084/jem.20110540
  • ISSN: 1540-9538; 0022-1007
  • Schlagwörter: Immunology ; Immunology and Allergy
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:p>The molecular pathophysiology of myeloproliferative neoplasms (MPNs) remains poorly understood. Based on the observation that the transcription factor NF-E2 is often overexpressed in MPN patients, independent of the presence of other molecular aberrations, we generated mice expressing an NF-E2 transgene in hematopoietic cells. These mice exhibit many features of MPNs, including thrombocytosis, leukocytosis, Epo-independent colony formation, characteristic bone marrow histology, expansion of stem and progenitor compartments, and spontaneous transformation to acute myeloid leukemia. The MPN phenotype is transplantable to secondary recipient mice. NF-E2 can alter histone modifications, and NF-E2 transgenic mice show hypoacetylation of histone H3. Treatment of mice with the histone deacetylase inhibitor (HDAC-I) vorinostat restored physiological levels of histone H3 acetylation, decreased NF-E2 expression, and normalized platelet numbers. Similarly, MPN patients treated with an HDAC-I exhibited a decrease in NF-E2 expression. These data establish a role for NF-E2 in the pathophysiology of MPNs and provide a molecular rationale for investigating epigenetic alterations as novel targets for rationally designed MPN therapies.</jats:p>
  • Zugangsstatus: Freier Zugang