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J Exp Med. 2019 Oct 7;216(10):2362-2377. doi: 10.1084/jem.20190598. Epub 2019 Aug 1.

CD97 is a critical regulator of acute myeloid leukemia stem cell function.

Author information

1
Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY.
2
Department of Pathology, New York University School of Medicine, New York, NY.
3
Leukemia Service, Memorial Sloan Kettering Cancer Center, New York, NY.
4
Department of Medicine, Division of Hematology/Oncology, University of Virginia, Charlottesville, VA.
5
Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA.
6
Department of Medicine, Division of Hematology/Oncology, Weill Cornell Medicine, New York, NY.
7
Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands.
8
Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY.
9
Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY.
10
Department of Pathology, New York University School of Medicine, New York, NY christopher.park@nyulangone.org.

Abstract

Despite significant efforts to improve therapies for acute myeloid leukemia (AML), clinical outcomes remain poor. Understanding the mechanisms that regulate the development and maintenance of leukemic stem cells (LSCs) is important to reveal new therapeutic opportunities. We have identified CD97, a member of the adhesion class of G protein-coupled receptors (GPCRs), as a frequently up-regulated antigen on AML blasts that is a critical regulator of blast function. High levels of CD97 correlate with poor prognosis, and silencing of CD97 reduces disease aggressiveness in vivo. These phenotypes are due to CD97's ability to promote proliferation, survival, and the maintenance of the undifferentiated state in leukemic blasts. Collectively, our data credential CD97 as a promising therapeutic target on LSCs in AML.

PMID:
31371381
PMCID:
PMC6781010
[Available on 2020-04-07]
DOI:
10.1084/jem.20190598

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