ReviewMolecular cancer2018
Mechanisms of receptor tyrosine kinase activation in cancer.
Review in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 555 papers, 1 of them a synthesis that pooled it.
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
555 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,039 citations in OpenAlex.
- Genetic characteristics and targeted treatments of primary bladder and urachal adenocarcinomas: a systematic review with pooled descriptive genomic analyses.Cancer metastasis reviews · 2026Pooled it
- The effect of food on the pharmacokinetics of Sutetinib maleate capsule, an irreversible EGFR tyrosine kinase inhibitor, in healthy Chinese subjects.Investigational new drugs · 2024Trial
- Targeting receptor tyrosine kinases: from molecular mechanisms to clinical therapeutics.Signal transduction and targeted therapy · 2026Review
- DDR1 sustains ferroptosis resistance in pancreatic ductal adenocarcinoma via SLC40A1-mediated iron homeostasis.Oncogene · 2026Article
- Next-generation multiplexed targeted proteomics quantifies post-translational modifications in disease and compound-protein interactions with high throughput.Nature communications · 2026Article
- TogoPhosTAC as a delivery-ready platform for targeted protein dephosphorylation.Nature communications · 2026Article
- Evaluation of the Biological Potential of an EndophyticMicroorganisms · 2026Article
- Recent Progress in Urea-Containing Compounds as Tyrosine Kinase Inhibitors.Chemistry & biodiversity · 2026Review
- Nanobody-based targeted cancer therapy and immunotherapy: fear not the future.Acta pharmacologica Sinica · 2026Review
- Scalable phosphotyrosine enrichment with SH2 superbinder enables deep profiling of EGF responses.The EMBO journal · 2026Article
- Evolving Landscape of Systemic Therapy for Hepatocellular Carcinoma: From Targeted Therapy and Combination Strategies to Emerging Therapies.Biomedicines · 2026Review
- Advances in the design and discovery of small-molecule tyrosine kinase inhibitors for breast cancer.RSC advances · 2026Review
- Review
- Opportunities and challenges in the development of evolving EGFR inhibitors to overcome EGFR TKIs resistance.Acta pharmacologica Sinica · 2026Review
- Tyrosine Kinase Receptors, Inhibition, and Potential Role in the Pharmacotherapy of Retinal Disorders.Ophthalmology and therapy · 2026Review
- Targeting non-small cell lung cancer: Molecular mechanisms and clinical studies (Review).Oncology letters · 2026Review
- Genomic structural equation modelling of 12 cancers identifies a latent pan-cancer susceptibility factor and shared determinants of carcinogenesis.EBioMedicine · 2026Article
- EphA2 as an oncogenic driver: roles and mechanisms of action in cancer.Molecular biology reports · 2026Review
- Engineering a Transmembrane Receptor for Coacervate-Based Artificial Cells.Journal of the American Chemical Society · 2026Article
- In vitro and in silico modelling of ROS1-positive non-small cell lung cancer reveals fusion-dependent tyrosine kinase inhibitor responses.Molecular oncology · 2026Article
495 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Receptor tyrosine kinases (RTKs) play an important role in a variety of cellular processes including growth, motility, differentiation, and metabolism. As such, dysregulation of RTK signaling leads to an assortment of human diseases, most notably, cancers. Recent large-scale genomic studies have revealed the presence of various alterations in the genes encoding RTKs such as EGFR, HER2/ErbB2, and MET, amongst many others. Abnormal RTK activation in human cancers is mediated by four principal mechanisms: gain-of-function mutations, genomic amplification, chromosomal rearrangements, and / or autocrine activation. In this manuscript, we review the processes whereby RTKs are activated under normal physiological conditions and discuss several mechanisms whereby RTKs can be aberrantly activated in human cancers. Understanding of these mechanisms has important implications for selection of anti-cancer therapies.
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.