@article{6c927096cd4b490bb60ccb5546fa9336,
title = "EPHB4 is a therapeutic target in AML and promotes leukemia cell survival via AKT",
abstract = "EPHB4, an ephrin type B receptor, is implicated in the growth of several epithelial tumors and is a promising target in cancer therapy; however, little is known about its role in hematologic malignancies. In this article, we show that EPHB4 is highly expressed in;30% of acute myeloid leukemia (AML) samples. In an unbiased RNA interference screen of primary leukemia samples, we found that EPHB4 drives survival in a subset of AML cases. Knockdown of EPHB4 inhibits phosphatidylinositol 3-kinase/AKT signaling, and this is accompanied by a reduction in cell viability, which can be rescued by a constitutively active form of AKT. Finally, targeting EPHB4 with a highly specific monoclonal antibody (MAb131) is effective against AML in vitro and in vivo. EPHB4 is therefore a potential target in AML with high EPHB4 expression.",
author = "Merchant, {Akil A.} and Aparna Jorapur and Amy McManus and Ren Liu and Valery Krasnoperov and Parvesh Chaudhry and Mohan Singh and Lisa Harton and Mary Agajanian and Miriam Kim and Triche, {Timothy J.} and Druker, {Brian J.} and Tyner, {Jeffrey W.} and Gill, {Parkash S.}",
note = "Funding Information: This work was supported in part by award P30CA014089 and career development award K08 CA154975-01A1 (A.A.M.) from the National Institutes of Health, National Cancer Institute. J.W.T. was supported by the Leukemia and Lymphoma Society, the V Foundation for Cancer Research, the Gabrielle{\textquoteright}s Angel Foundation for Cancer Research, and the National Institutes of Health, National Cancer Institute (grants 5R00CA151457-04 and 1R01CA183947-01). Publisher Copyright: {\textcopyright} 2017 by The American Society of Hematology.",
year = "2017",
month = sep,
day = "12",
doi = "10.1182/bloodadvances.2017005694",
language = "English",
volume = "1",
pages = "1635--1644",
journal = "Blood Advances",
issn = "2473-9529",
number = "20",
}