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

The Journal of Experimental Medicine
Gaëlle H MartinChristopher Y Park

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.

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Citations

Nov 5, 2020·Blood Advances·Jenny M HoJean C Y Wang
May 8, 2021·Neuro-oncology Advances·Gabriele StephanDimitris G Placantonakis
Sep 11, 2021·Frontiers in Molecular Biosciences·Huiqing Qu, Ye Zhu
Sep 2, 2021·Blood Advances·Paraskevi DiamantiAllison Blair
Nov 4, 2021·The FEBS Journal·Ines LiebscherSimone Prömel

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Datasets Mentioned

BETA
GSM909310

Methods Mentioned

BETA
flow cytometry
RNA-seq
antibody array
density gradient centrifugation
PCR
antisense oligonucleotides

Clinical Trials Mentioned

NCT02678338

Software Mentioned

Ingenuity Pathways Analysis ( IPA )
TreeStar
Flowjo
Gene Ontology Panther
R
Gene
Rsamtools
ELDA
DESeq2
GSEA

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