ArticleOncotarget2015
Mer receptor tyrosine kinase is frequently overexpressed in human non-small cell lung cancer, confirming resistance to erlotinib.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 46 citations in OpenAlex.
- A MERTK-Targeting Antibody-Drug Conjugate Selectively Depletes M2 Tumor-Associated Macrophages and MERTK-Expressing Cancer Cells.Cancer research · 2026Article
- STK38 Kinase Promotes Cell Migration Induced by Oncogenic Ras via MerTK Activation.International journal of molecular sciences · 2025Article
- The role of tumor-associated macrophages in lung cancer.Frontiers in immunology · 2025Review
- Efficacy and Safety of Amivantamab in Advanced or Metastatic EGFR-Mutant Non-Small Cell Lung Cancer: A Systematic Review.Journal of clinical medicine · 2024Review
- Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024Review
- MERTK Inhibition as a Targeted Novel Cancer Therapy.International journal of molecular sciences · 2024Review
- MERTK activation drives osimertinib resistance in EGFR-mutant non-small cell lung cancer.The Journal of clinical investigation · 2022Article
- Macrophages Are a Double-Edged Sword: Molecular Crosstalk between Tumor-Associated Macrophages and Cancer Stem Cells.Biomolecules · 2022Review
- Review
- [Advances in the Study of Tumor-associated Macrophages in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2022Review
- Efferocytosis in multisystem diseases (Review).Molecular medicine reports · 2022Review
- Mertk: An emerging target in cancer biology and immuno-oncology.International review of cell and molecular biology · 2022Article
- Targeting MERTK and AXL inCancers · 2021Review
- A narrative review of tumor-associated macrophages in lung cancer: regulation of macrophage polarization and therapeutic implications.Translational lung cancer research · 2021Review
- MERTK Inhibition: Potential as a Treatment Strategy in EGFR Tyrosine Kinase Inhibitor-Resistant Non-Small Cell Lung Cancer.Pharmaceuticals (Basel, Switzerland) · 2021Review
- TAM kinase inhibition and immune checkpoint blockade- a winning combination in cancer treatment?Expert opinion on therapeutic targets · 2021Review
- AXL Receptor in Breast Cancer: Molecular Involvement and Therapeutic Limitations.International journal of molecular sciences · 2020Review
- MERTK in cancer therapy: Targeting the receptor tyrosine kinase in tumor cells and the immune system.Pharmacology & therapeutics · 2020Review
- Early urinary protein changes during tumor formation in a NuTu-19 tail vein injection rat model.Scientific reports · 2020Article
- Identification of anaplastic lymphoma kinase fusions in clear cell renal cell carcinoma.Oncology reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mer is a receptor tyrosine kinase (RTK) with oncogenic properties that is often overexpressed or activated in various malignancies. Using both immunohistochemistry and microarray analyses, we demonstrated that Mer was overexpressed in both tumoral and stromal compartments of about 70% of non-small cell lung cancer (NSCLC) samples relative to surrounding normal lung tissue. This was validated in freshly harvested NSCLC samples; however, no associations were found between Mer expression and patient features. Although Mer overexpression did not render normal lung epithelial cell tumorigenic in vivo, it promoted the in vitro cell proliferation, clonogenic colony formation and migration of normal lung epithelial cells as well as NSCLC cells primarily depending on MAPK and FAK signaling, respectively. Importantly, Mer overexpression induced resistance to erlotinib (EGFR inhibitor) in otherwise erlotinib-sensitive cells. Furthermore, Mer-specific inhibitor rendered erlotinib-resistant cells sensitive to erlotinib. We conclude that Mer enhances malignant phenotype and pharmacological inhibition of Mer overcomes resistance of NSCLC to EGFR-targeted agents.
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.