Academic Journal

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

التفاصيل البيبلوغرافية
العنوان: CD97 is a critical regulator of acute myeloid leukemia stem cell function
المؤلفون: 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.
المساهمون: Leukemia and Lymphoma Society, New York State Stem Cell Science, National Cancer Institute, American Society of Hematology
المصدر: Journal of Experimental Medicine ; volume 216, issue 10, page 2362-2377 ; ISSN 0022-1007 1540-9538
بيانات النشر: Rockefeller University Press
سنة النشر: 2019
الوصف: 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.
نوع الوثيقة: article in journal/newspaper
اللغة: English
DOI: 10.1084/jem.20190598
الاتاحة: http://dx.doi.org/10.1084/jem.20190598
https://rupress.org/jem/article-pdf/216/10/2362/1765730/jem_20190598.pdf
Rights: http://www.rupress.org/terms/ ; https://creativecommons.org/licenses/by-nc-sa/4.0/
رقم الانضمام: edsbas.2DA3E6CE
قاعدة البيانات: BASE