期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 216, 期 10, 页码 2362-2377出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20190598
关键词
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资金
- Leukemia and Lymphoma Society
- New York State Stem Cell Science institutional training grant (NYSTEM) [C32560GG]
- National Cancer Institute [K08CA169055]
- American Society of Hematology under the American Society of Hematology-Harold Amos Medical Faculty Development Program [ASHAMFDP-20121]
- Robert Wood Johnson Foundation
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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