Hmga2 collaborates with JAK2V617F in the development of myeloproliferative neoplasms

Author:

Ueda Koki1,Ikeda Kazuhiko12,Ikezoe Takayuki1,Harada-Shirado Kayo12,Ogawa Kazuei1,Hashimoto Yuko3,Sano Takahiro1,Ohkawara Hiroshi1,Kimura Satoshi1,Shichishima-Nakamura Akiko1,Nakamura Yuichi4,Shikama Yayoi5,Mori Tsutomu6,Mason Philip J.7,Bessler Monica7,Morishita Soji8,Komatsu Norio8,Shide Kotaro9,Shimoda Kazuya9,Koide Shuhei10,Aoyama Kazumasa10,Oshima Motohiko10,Iwama Atsushi10,Takeishi Yasuchika4

Affiliation:

1. Department of Hematology,

2. Department of Blood Transfusion and Transplantation Immunology,

3. Department of Diagnostic Pathology,

4. Department of Cardiovascular Medicine, and

5. Department of Pharmacology, Fukushima Medical University, Fukushima, Japan;

6. Department of Human Lifesciences, Fukushima Medical University School of Nursing, Fukushima, Japan;

7. Department of Hematology, The Children’s Hospital of Philadelphia, Philadelphia, PA;

8. Department of Hematology, Juntendo University School of Medicine, Tokyo, Japan;

9. Department of Gastroenterology and Hematology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan; and

10. Department of Cellular and Molecular Medicine, Chiba University Graduate School of Medicine, Chiba, Japan

Abstract

Key Points In patients with MPNs, repression of MIRlet-7 and mutations in the polycomb genes EZH2 and ASXL1 correlate with HMGA2 overexpression. Hmga2 overexpression collaborates with JAK2V617F to promote lethal MPN in mice, highlighting the crucial role of Hmga2.

Publisher

American Society of Hematology

Subject

Hematology

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