Effects of the leukemia-associated AML1-ETO protein on hematopoietic stem and progenitor cells

Stephen D. Nimer; Malcolm A.S. Moore

doi:10.1038/sj.onc.1207673

Effects of the leukemia-associated AML1-ETO protein on hematopoietic stem and progenitor cells

Stephen D. Nimer, Malcolm A.S. Moore

Research output: Contribution to journal › Review article › peer-review

47 Scopus citations

Abstract

Insights into the pathogenesis of human leukemia have relied heavily on studies of the identified chromosomal translocations found in this group of malignant diseases. Acquired, balanced translocations in acute myclogenous leukemia (AML) generally involve transcriptional regulatory genes, whereas in the myeloproliferative disorders tyrosine kinases are frequently involved. These rearrangements alter the function of at least one and often both of the involved genes. In this review, we focus on the AML1-ETO (a.k.a. RUNX1-ETO) fusion protein, which is found in t(8;21) + AML. Expression of AML1-ETO in human hematopoietic stem cells (HSCs) preferentially enhances their maintenance, as opposed to their differentiation. The direct effects of AML1-ETO on human and murine HSCs, and the potentially cooperating events that may contribute to its leukemogenic properties, are discussed.

Original language	English (US)
Pages (from-to)	4249-4254
Number of pages	6
Journal	Oncogene
Volume	23
Issue number	24
DOIs	https://doi.org/10.1038/sj.onc.1207673
State	Published - May 24 2004
Externally published	Yes

Keywords

AML
AML1-ETO
Stem cell biology
Transcription factors

ASJC Scopus subject areas

Molecular Biology
Cancer Research
Genetics

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title = "Effects of the leukemia-associated AML1-ETO protein on hematopoietic stem and progenitor cells",

abstract = "Insights into the pathogenesis of human leukemia have relied heavily on studies of the identified chromosomal translocations found in this group of malignant diseases. Acquired, balanced translocations in acute myclogenous leukemia (AML) generally involve transcriptional regulatory genes, whereas in the myeloproliferative disorders tyrosine kinases are frequently involved. These rearrangements alter the function of at least one and often both of the involved genes. In this review, we focus on the AML1-ETO (a.k.a. RUNX1-ETO) fusion protein, which is found in t(8;21) + AML. Expression of AML1-ETO in human hematopoietic stem cells (HSCs) preferentially enhances their maintenance, as opposed to their differentiation. The direct effects of AML1-ETO on human and murine HSCs, and the potentially cooperating events that may contribute to its leukemogenic properties, are discussed.",

keywords = "AML, AML1-ETO, Stem cell biology, Transcription factors",

author = "Nimer, {Stephen D.} and Moore, {Malcolm A.S.}",

note = "Funding Information: This work was supported by a Leukemia, Lymphoma Society Specialized Center of Research Grant. We thank Ms Ellie Park for her assistance in the preparation of this paper. We also wish to express our profound sadness over the recent death of our friend, Dr Hisamaru Hirai, a leader in the laboratory and clinical investigation of leukemia and MDS.",

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AU - Moore, Malcolm A.S.

N1 - Funding Information: This work was supported by a Leukemia, Lymphoma Society Specialized Center of Research Grant. We thank Ms Ellie Park for her assistance in the preparation of this paper. We also wish to express our profound sadness over the recent death of our friend, Dr Hisamaru Hirai, a leader in the laboratory and clinical investigation of leukemia and MDS.

PY - 2004/5/24

Y1 - 2004/5/24

N2 - Insights into the pathogenesis of human leukemia have relied heavily on studies of the identified chromosomal translocations found in this group of malignant diseases. Acquired, balanced translocations in acute myclogenous leukemia (AML) generally involve transcriptional regulatory genes, whereas in the myeloproliferative disorders tyrosine kinases are frequently involved. These rearrangements alter the function of at least one and often both of the involved genes. In this review, we focus on the AML1-ETO (a.k.a. RUNX1-ETO) fusion protein, which is found in t(8;21) + AML. Expression of AML1-ETO in human hematopoietic stem cells (HSCs) preferentially enhances their maintenance, as opposed to their differentiation. The direct effects of AML1-ETO on human and murine HSCs, and the potentially cooperating events that may contribute to its leukemogenic properties, are discussed.

AB - Insights into the pathogenesis of human leukemia have relied heavily on studies of the identified chromosomal translocations found in this group of malignant diseases. Acquired, balanced translocations in acute myclogenous leukemia (AML) generally involve transcriptional regulatory genes, whereas in the myeloproliferative disorders tyrosine kinases are frequently involved. These rearrangements alter the function of at least one and often both of the involved genes. In this review, we focus on the AML1-ETO (a.k.a. RUNX1-ETO) fusion protein, which is found in t(8;21) + AML. Expression of AML1-ETO in human hematopoietic stem cells (HSCs) preferentially enhances their maintenance, as opposed to their differentiation. The direct effects of AML1-ETO on human and murine HSCs, and the potentially cooperating events that may contribute to its leukemogenic properties, are discussed.

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KW - Stem cell biology

KW - Transcription factors

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Effects of the leukemia-associated AML1-ETO protein on hematopoietic stem and progenitor cells

Abstract

Keywords

ASJC Scopus subject areas

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