ArticleBlood advances2017
EPHB4 is a therapeutic target in AML and promotes leukemia cell survival via AKT.
Article in Blood advances, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Eph receptors and ephrins in cancer progression.Nature reviews. Cancer · 2024Review
- Review
- Vandetanib drives growth arrest and promotes sensitivity to imatinib in chronic myeloid leukemia by targeting ephrin type-B receptor 4.Molecular oncology · 2022Article
- EphB4 as a Novel Target for the EGFR-Independent Suppressive Effects of Osimertinib on Cell Cycle Progression in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2021Article
- Review
- Current Advances inFrontiers in pharmacology · 2021Review
- Critical role of EphA3 in cancer and current state of EphA3 drug therapeutics.Molecular biology reports · 2020Review
- Antibody Targeting of Eph Receptors in Cancer.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Leukemia Stem Cell Release From the Stem Cell Niche to Treat Acute Myeloid Leukemia.Frontiers in cell and developmental biology · 2020Review
- Emerging Roles for Eph Receptors and Ephrin Ligands in Immunity.Frontiers in immunology · 2019Review
- Therapeutic potential of targeting the Eph/ephrin signaling complex.The international journal of biochemistry & cell biology · 2018Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
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
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.