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

Gaëlle H. Martin, Nainita Roy, Sohini Chakraborty, Alexis Desrichard, Stephen S. Chung, Carolien M. Woolthuis, Wenhuo Hu, Iryna Berezniuk, Francine E. Garrett-Bakelman, Jörg Hamann, Sean M. Devlin, Timothy A. Chan, Christopher Y. Park

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)2362-2377
Number of pages16
JournalThe Journal of experimental medicine
Volume216
Issue number10
DOIs
StatePublished - Oct 7 2019

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'CD97 is a critical regulator of acute myeloid leukemia stem cell function'. Together they form a unique fingerprint.

Cite this