ArticleScientific reports2015
Novel EPHB4 Receptor Tyrosine Kinase Mutations and Kinomic Pathway Analysis in Lung Cancer.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 25 citations in OpenAlex.
- Identification of Ephrin type-B receptor 4 as a critical mediator of tissue fibrosis.JCI insight · 2025Article
- Germline alteration analysis reveals EPHB4R91H mutation as a key player in multiple primary lung tumors.Carcinogenesis · 2025Article
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- Ephs in cancer progression: complexity and context-dependent nature in signaling, angiogenesis and immunity.Cell communication and signaling : CCS · 2024Review
- Mucinous adenocarcinoma caused by cancerization from a ciliated multinodular papilloma tumor: A case report.Thoracic cancer · 2021Article
- Kinome multigenic panel identified novel druggable EPHB4-V871I somatic variant in high-risk neuroblastoma.Journal of cellular and molecular medicine · 2020Article
- EPHA2 mutations with oncogenic characteristics in squamous cell lung cancer and malignant pleural mesothelioma.Oncogenesis · 2019Article
- Article
- Mutations in Chromatin Modifier and Ephrin Signaling Genes in Vein of Galen Malformation.Neuron · 2019Article
- Modeling small cell lung cancer (SCLC) biology through deterministic and stochastic mathematical models.Oncotarget · 2018Review
- Genomic alterations of ground-glass nodular lung adenocarcinoma.Scientific reports · 2018Article
- EphB4: A promising target for upper aerodigestive malignancies.Biochimica et biophysica acta. Reviews on cancer · 2018Review
- Proteomic approach toward determining the molecular background of pazopanib resistance in synovial sarcoma.Oncotarget · 2017Article
- EPHB4 is a therapeutic target in AML and promotes leukemia cell survival via AKT.Blood advances · 2017Article
- Cetuximab Prevents Methotrexate-Induced Cytotoxicity in Vitro through Epidermal Growth Factor Dependent Regulation of Renal Drug Transporters.Molecular pharmaceutics · 2017Article
- Enhancing radiosensitization in EphB4 receptor-expressing Head and Neck Squamous Cell Carcinomas.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer outcomes remain poor despite the identification of several potential therapeutic targets. The EPHB4 receptor tyrosine kinase (RTK) has recently emerged as an oncogenic factor in many cancers, including lung cancer. Mutations of EPHB4 in lung cancers have previously been identified, though their significance remains unknown. Here, we report the identification of novel EPHB4 mutations that lead to putative structural alterations as well as increased cellular proliferation and motility. We also conducted a bioinformatic analysis of these mutations to demonstrate that they are mutually exclusive from other common RTK variants in lung cancer, that they correspond to analogous sites of other RTKs' variations in cancers, and that they are predicted to be oncogenic based on biochemical, evolutionary, and domain-function constraints. Finally, we show that EPHB4 mutations can induce broad changes in the kinome signature of lung cancer cells. Taken together, these data illuminate the role of EPHB4 in lung cancer and further identify EPHB4 as a potentially important therapeutic target.
Indexed as
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.