FLT3 activation cooperates with MLL-AF4 fusion protein to abrogate the hematopoietic specification of human ESCs-Reference-Cited by-同舟云学术

FLT3 activation cooperates with MLL-AF4 fusion protein to abrogate the hematopoietic specification of human ESCs

Published:2013-05-09 Issue:19 Volume:121 Page:3867-3878
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Bueno Clara¹,Ayllón Verónica¹,Montes Rosa¹,Navarro-Montero Oscar¹,Ramos-Mejia Verónica¹,Real Pedro J.¹,Romero-Moya Damià¹,Araúzo-Bravo Marcos J.²,Menendez Pablo¹³⁴

Affiliation:

1. Centre for Genomics and Oncological Research, Pfizer-University of Granada-Andalusian Regional Government, Granada, Spain;

2. Max Planck Institute for Molecular Biomedicine, Department of Cell and Developmental Biology, Laboratory of Computational Biology and Bioinformatics, Muenster, Germany;

3. Josep Carreras Leukemia Research Institute and Cell Therapy Program, Facultat de Medicina, University of Barcelona, Spain;

4. Instituciò Catalana de Reserca i Estudis Avançats (ICREA), Barcelona, Spain

Abstract

Key Points FLT3 activation cooperates with the MLL-AF4 fusion gene to fully abolish blood formation from hESCs. FLT3 activation does not cooperate with the MLL-AF4 fusion oncogene to transform hESCs or hESC-derived hematopoietic progeny.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/121/19/3867/1218576/3867.pdf

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4. MLL translocations, histone modifications and leukaemia stem-cell development.;Krivtsov;Nat Rev Cancer,2007

5. In utero rearrangements in the trithorax-related oncogene in infant leukaemias.;Ford;Nature,1993

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