期刊
BLOOD
卷 127, 期 16, 页码 2018-2027出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2015-11-683649
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资金
- Cancer Research Network of the Fonds de Recherche du Quebec en Sante
- Government of Canada through Genome Canada
- Ministere de l'economie, de l'innovation et de l'exportation du Quebec through Genome Quebec
- Canada Research Chair in Molecular Genetics of Stem Cells
- Research Chair in Leukemia - Industrielle-Alliance (Universite de Montreal)
- German Cancer Aid (Deutsche Krebshilfe)
- Cole Foundation
- Max-Eder-Grant from the German Cancer Aid
- Vetenskapsradet
Acute myeloid leukemia (AML) is a genetically heterogeneous hematologic malignancy, which is initiated and driven by a rare fraction of leukemia stem cells (LSCs). Despite the difficulties of identifying a common LSC phenotype, there is increasing evidence that high expression of stem cell gene signatures is associated with poor clinical outcome. Identification of functionally distinct subpopulations in this disease is therefore crucial to dissecting the molecular machinery underlying LSC self-renewal. Here, we combined next-generation sequencing technology with in vivo assessment of LSC frequencies and identified the adhesion G protein-coupled receptor 56 (GPR56) as a novel and stable marker for human LSCs for the majority of AML samples. High GPR56 expression was significantly associated with high-risk genetic subgroups and poor outcome. Analysis of GPR56 in combination with CD34 expression revealed engraftment potential of GPR56(+) cells in both the CD34(-) and CD34(+) fractions, thus defining a novel LSC compartment independent of the CD34(+) CD38(-) LSC phenotype.
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