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


Authors: Martin, G. H.; Roy, N.; Chakraborty, S.; Desrichard, A.; Chung, S. S.; Woolthuis, C. M.; Hu, W.; Berezniuk, I.; Garrett-Bakelman, F. E.; Hamann, J.; Devlin, S. M.; Chan, T. A.; Park, C. Y.
Article Title: CD97 is a critical regulator of acute myeloid leukemia stem cell function
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. © 2019 Martin et al.
Journal Title: Journal of Experimental Medicine
Volume: 216
Issue: 10
ISSN: 0022-1007
Publisher: Rockefeller University Press  
Date Published: 2019-10-01
Start Page: 2362
End Page: 2377
Language: English
DOI: 10.1084/jem.20190598
PUBMED: 31371381
PROVIDER: scopus
PMCID: PMC6781010
DOI/URL:
Notes: Source: Scopus
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  1. Timothy Chan
    317 Chan
  2. Stephen Shiu-Wah Chung
    61 Chung
  3. Wenhuo Hu
    60 Hu
  4. Sean McCarthy Devlin
    601 Devlin
  5. Gaelle Gilberte Helene Martin
    2 Martin