Journal
CANCER CELL
Volume 30, Issue 5, Pages 792-805Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2016.10.003
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Funding
- National Cancer Center
- Japanese Society for the Promotion of Science
- NIH [T32 GM007752, HL078784, HL117807, HL097767, DK099335, DP1 CA174422, R35 CA197699]
- National Research Service Award [F31 CA206416]
- Arthritis Foundation
- Melanoma Research Alliance
- Lymphoma and Leukemia Society
- Grants-in-Aid for Scientific Research [16K19570] Funding Source: KAKEN
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Acute myelogenous leukemia (AML) is an aggressive disease associated with drug resistance and relapse. To improve therapeutic strategies, it is critical to better understand the mechanisms that underlie AML progression. Here we show that the integrin binding glycoprotein CD98 plays a central role in AML. CD98 promotes AML propagation and lethality by driving engagement of leukemia cells with their microenvironment and maintaining leukemic stem cells. Further, delivery of a humanized anti-CD98 antibody blocks growth of patient -derived AML, highlighting the importance of this pathway in human disease. These findings indicate that microenvironmental interactions are key regulators of AML and that disrupting these signals with targeted inhibitors such as CD98 antibodies may be a valuable therapeutic approach for adults and children with this disease.
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