GATA2 haploinsufficiency accelerates EVI1-driven leukemogenesis-Reference-Cited by-同舟云学术

GATA2 haploinsufficiency accelerates EVI1-driven leukemogenesis

Published:2017-08-17 Issue:7 Volume:130 Page:908-919
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Katayama Saori¹²,Suzuki Mikiko³,Yamaoka Ayaka¹,Keleku-Lukwete Nadine¹,Katsuoka Fumiki⁴,Otsuki Akihito⁵,Kure Shigeo²,Engel James Douglas⁶,Yamamoto Masayuki¹⁶

Affiliation:

1. Department of Medical Biochemistry,

2. Department of Pediatrics, and

3. Center for Radioisotope Sciences, Tohoku University Graduate School of Medicine, Sendai, Japan;

4. Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan;

5. Division of Medical Biochemistry, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Japan; and

6. Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI

Abstract

Key Points Leukemic cells in an inv(3)(q21q26) EVI1 misexpression mouse model are able to differentiate toward myeloid lineage. Gata2 heterozygous deletion accelerates EVI1 misexpression leukemia by inducing a proliferation and differentiation defect in leukemia cells.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/130/7/908/1367519/blood756767.pdf

Reference37 articles.

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4. Evi1 represses PTEN expression and activates PI3K/AKT/mTOR via interactions with polycomb proteins;Yoshimi;Blood,2011

5. A remote GATA2 hematopoietic enhancer drives leukemogenesis in inv(3)(q21;q26) by activating EVI1 expression;Yamazaki;Cancer Cell,2014

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