ArticleOncotarget2014
MerTK inhibition is a novel therapeutic approach for glioblastoma multiforme.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 60 citations in OpenAlex.
- MerTK inhibition by UNC569 triggers DNA damage and JNK/p38 MAPK cascade-driven apoptosis in pancreatic cancer.Acta biochimica et biophysica Sinica · 2026Article
- Preclinical evaluation of CPL423: a novel potent small-molecule inhibitor of TAM family and FLT3 kinase for cancer therapy.Frontiers in pharmacology · 2026Article
- STK38 Kinase Promotes Cell Migration Induced by Oncogenic Ras via MerTK Activation.International journal of molecular sciences · 2025Article
- Establishment and characterization of NCC-SFT1-C1: a novel patient-derived cell line of solitary fibrous tumor.Human cell · 2025Article
- MERTK Inhibition as a Targeted Novel Cancer Therapy.International journal of molecular sciences · 2024Review
- Molecular signature of stem-like glioma cells (SLGCs) from human glioblastoma and gliosarcoma.PloS one · 2024Article
- Preclinical Evaluation of Trabectedin in Combination With Targeted Inhibitors for Treatment of Metastatic Uveal Melanoma.Investigative ophthalmology & visual science · 2022Article
- Patient-Derived Tumor Organoids for Guidance of Personalized Drug Therapies in Recurrent Glioblastoma.International journal of molecular sciences · 2022Article
- Review
- Novel Receptor Tyrosine Kinase Pathway Inhibitors for Targeted Radionuclide Therapy of Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Foretinib induces G2/M cell cycle arrest, apoptosis, and invasion in human glioblastoma cells through c-MET inhibition.Cancer chemotherapy and pharmacology · 2021Article
- Immuno-oncology: are TAM receptors in glioblastoma friends or foes?Cell communication and signaling : CCS · 2021Review
- MERTK in cancer therapy: Targeting the receptor tyrosine kinase in tumor cells and the immune system.Pharmacology & therapeutics · 2020Review
- Macrophages Orchestrate Hematopoietic Programs and Regulate HSC Function During Inflammatory Stress.Frontiers in immunology · 2020Review
- TYRO3: A potential therapeutic target in cancer.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Receptor tyrosine kinase-Ras-PI 3 kinase-Akt signaling network in glioblastoma multiforme.Medical oncology (Northwood, London, England) · 2018Review
- The role of TAM family receptors and ligands in the nervous system: From development to pathobiology.Pharmacology & therapeutics · 2018Review
- Signaling pathways and mesenchymal transition in pediatric high-grade glioma.Cellular and molecular life sciences : CMLS · 2018Review
- Article
- 5-Aminolevulinic Acid Guided Sampling of Glioblastoma Microenvironments Identifies Pro-Survival Signaling at Infiltrative Margins.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Glioblastoma is an aggressive tumor that occurs in both adult and pediatric patients and is known for its invasive quality and high rate of recurrence. Current therapies for glioblastoma result in high morbidity and dismal outcomes. The TAM subfamily of receptor tyrosine kinases includes Tyro3, Axl, and MerTK. Axl and MerTK exhibit little to no expression in normal brain but are highly expressed in glioblastoma and contribute to the critical malignant phenotypes of survival, chemosensitivity and migration. We have found that Foretinib, a RTK inhibitor currently in clinical trial, inhibited phosphorylation of TAM receptors, with highest efficacy against MerTK, and blocked downstream activation of Akt and Erk in adult and pediatric glioblastoma cell lines, findings that are previously unreported. Survival, proliferation, migration, and collagen invasion were hindered in vitro. Foretinib treatment in vivo abolished MerTK phosphorylation and reduced tumor growth 3-4 fold in a subcutaneous mouse model. MerTK targeted shRNA completely prevented intracranial and subcutaneous glioma growth further delineating the impact of MerTK inhibition on glioblastoma. Our findings provide additional target validation for MerTK inhibition in glioblastoma and demonstrate that robust MerTK inhibition can be achieved with the multi-kinase inhibitor Foretinib as an innovative and translational therapeutic approach to glioblastoma.
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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.