ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia

ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia

While the role of ASLX1 in haematopoiesis and leukaemia has been heavily studied, the role of ASLX2 is unclear. Here the authors show that ASLX2 is required for normal haematopoietic stem cell self-renewal whereas Asxl2 loss promotes leukemogenesis, thus explaining the frequently observed mutations...

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Main Authors: Jean-Baptiste Micol, Alessandro Pastore, Daichi Inoue, Nicolas Duployez, Eunhee Kim, Stanley Chun-Wei Lee, Benjamin H. Durham, Young Rock Chung, Hana Cho, Xiao Jing Zhang, Akihide Yoshimi, Andrei Krivtsov, Richard Koche, Eric Solary, Amit Sinha, Claude Preudhomme, Omar Abdel-Wahab
Format: Article
Language:English
Published: Nature Publishing Group 2017-05-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/ncomms15429
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spelling doaj-4858a0bedd1541a2a819f03ad50874132021-05-11T07:24:22ZengNature Publishing GroupNature Communications2041-17232017-05-018111310.1038/ncomms15429ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemiaJean-Baptiste Micol0Alessandro Pastore1Daichi Inoue2Nicolas Duployez3Eunhee Kim4Stanley Chun-Wei Lee5Benjamin H. Durham6Young Rock Chung7Hana Cho8Xiao Jing Zhang9Akihide Yoshimi10Andrei Krivtsov11Richard Koche12Eric Solary13Amit Sinha14Claude Preudhomme15Omar Abdel-Wahab16Hematology Department, Inserm UMR1170, Gustave Roussy Cancer Campus Grand ParisHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical CollegeHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical CollegeLaboratory of Hematology and Tumor Bank, INSERM UMR-S 1172, Cancer Research Institute of Lille, CHRU of Lille, University Lille Nord de FranceSchool of Life Sciences, Ulsan National Institute of Science and TechnologyHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical CollegeHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical CollegeHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical CollegeHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical CollegeHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical CollegeHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical Collegeand Division of Hematology/Oncology, Dana-Farber Cancer Institute, Boston Children's Hospital, Harvard Medical SchoolCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer CenterHematology Department, Inserm UMR1170, Gustave Roussy Cancer Campus Grand ParisBasepair, Inc.Laboratory of Hematology and Tumor Bank, INSERM UMR-S 1172, Cancer Research Institute of Lille, CHRU of Lille, University Lille Nord de FranceHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical CollegeWhile the role of ASLX1 in haematopoiesis and leukaemia has been heavily studied, the role of ASLX2 is unclear. Here the authors show that ASLX2 is required for normal haematopoietic stem cell self-renewal whereas Asxl2 loss promotes leukemogenesis, thus explaining the frequently observed mutations in AML patientshttps://doi.org/10.1038/ncomms15429
collection DOAJ
language English
format Article
sources DOAJ
author Jean-Baptiste Micol
Alessandro Pastore
Daichi Inoue
Nicolas Duployez
Eunhee Kim
Stanley Chun-Wei Lee
Benjamin H. Durham
Young Rock Chung
Hana Cho
Xiao Jing Zhang
Akihide Yoshimi
Andrei Krivtsov
Richard Koche
Eric Solary
Amit Sinha
Claude Preudhomme
Omar Abdel-Wahab
spellingShingle Jean-Baptiste Micol
Alessandro Pastore
Daichi Inoue
Nicolas Duployez
Eunhee Kim
Stanley Chun-Wei Lee
Benjamin H. Durham
Young Rock Chung
Hana Cho
Xiao Jing Zhang
Akihide Yoshimi
Andrei Krivtsov
Richard Koche
Eric Solary
Amit Sinha
Claude Preudhomme
Omar Abdel-Wahab
ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia
Nature Communications
author_facet Jean-Baptiste Micol
Alessandro Pastore
Daichi Inoue
Nicolas Duployez
Eunhee Kim
Stanley Chun-Wei Lee
Benjamin H. Durham
Young Rock Chung
Hana Cho
Xiao Jing Zhang
Akihide Yoshimi
Andrei Krivtsov
Richard Koche
Eric Solary
Amit Sinha
Claude Preudhomme
Omar Abdel-Wahab
author_sort Jean-Baptiste Micol
title ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia
title_short ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia
title_full ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia
title_fullStr ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia
title_full_unstemmed ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia
title_sort asxl2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2017-05-01
description While the role of ASLX1 in haematopoiesis and leukaemia has been heavily studied, the role of ASLX2 is unclear. Here the authors show that ASLX2 is required for normal haematopoietic stem cell self-renewal whereas Asxl2 loss promotes leukemogenesis, thus explaining the frequently observed mutations in AML patients
url https://doi.org/10.1038/ncomms15429
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