| Literature DB >> 27908736 |
Jeevisha Bajaj1, Takaaki Konuma1, Nikki K Lytle1, Hyog Young Kwon1, Jailal N Ablack2, Joseph M Cantor2, David Rizzieri3, Charles Chuah4, Vivian G Oehler5, Elizabeth H Broome6, Edward D Ball7, Edward H van der Horst8, Mark H Ginsberg9, Tannishtha Reya10.
Abstract
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.Entities:
Keywords: CD98; SLC3A2; acute myelogenous leukemia; adhesion; cancer; cancer stem cell; imaging; integrin; leukemia; microenvironment
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Year: 2016 PMID： 27908736 PMCID： PMC5137811 DOI： 10.1016/j.ccell.2016.10.003
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743