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

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...

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Detalles Bibliográficos
Autores principales: Martin, Gaëlle H., Roy, Nainita, Chakraborty, Sohini, Desrichard, Alexis, Chung, Stephen S., Woolthuis, Carolien M., Hu, Wenhuo, Berezniuk, Iryna, Garrett-Bakelman, Francine E., Hamann, Jörg, Devlin, Sean M., Chan, Timothy A., Park, Christopher Y.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Rockefeller University Press 2019
Materias:
Research Articles
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781010/
https://www.ncbi.nlm.nih.gov/pubmed/31371381
http://dx.doi.org/10.1084/jem.20190598
Descripción
Sumario: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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