Molecular pathways driven by ETO2-GLIS2 in aggressive pediatric leukemia

Cécile Thirant; Cécile Lopez; Sébastien Malinge; Thomas Mercher

doi:10.1080/23723556.2017.1345351

Molecular pathways driven by ETO2-GLIS2 in aggressive pediatric leukemia

Cécile Thirant, Cécile Lopez, Sébastien Malinge, Thomas Mercher

Résultats de recherche: Contribution à un journal › Article › Revue par des pairs

10 Citations (Scopus)

Résumé

The ETO2-GLIS2 fusion oncoprotein is associated with poor prognosis pediatric acute megakaryoblastic leukemia. Recently, we observed that ETO2-GLIS2 controls enhancers activity at genes regulating haematopoietic progenitor self-renewal and differentiation toward the megakaryocytic lineage. We also showed that targeting ETO2-GLIS2 complex stability inhibits these properties and may represent a novel therapeutic strategy.

langue originale	Anglais
Numéro d'article	e1345351
journal	Molecular and Cellular Oncology
Volume	4
Numéro de publication	6
Les DOIs	https://doi.org/10.1080/23723556.2017.1345351
état	Publié - 2 nov. 2017

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10.1080/23723556.2017.1345351

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title = "Molecular pathways driven by ETO2-GLIS2 in aggressive pediatric leukemia",

abstract = "The ETO2-GLIS2 fusion oncoprotein is associated with poor prognosis pediatric acute megakaryoblastic leukemia. Recently, we observed that ETO2-GLIS2 controls enhancers activity at genes regulating haematopoietic progenitor self-renewal and differentiation toward the megakaryocytic lineage. We also showed that targeting ETO2-GLIS2 complex stability inhibits these properties and may represent a novel therapeutic strategy.",

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author = "C{\'e}cile Thirant and C{\'e}cile Lopez and S{\'e}bastien Malinge and Thomas Mercher",

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AB - The ETO2-GLIS2 fusion oncoprotein is associated with poor prognosis pediatric acute megakaryoblastic leukemia. Recently, we observed that ETO2-GLIS2 controls enhancers activity at genes regulating haematopoietic progenitor self-renewal and differentiation toward the megakaryocytic lineage. We also showed that targeting ETO2-GLIS2 complex stability inhibits these properties and may represent a novel therapeutic strategy.

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KW - GLIS2

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KW - enhancer

KW - leukemia

KW - transcription factor

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