ReviewDrug discovery today2017
Exploiting receptor tyrosine kinase co-activation for cancer therapy.
Review in Drug discovery today, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 37 citations in OpenAlex.
- Modeling acquired TKI resistance and effective combination therapeutic strategies in murine RET+ lung adenocarcinoma.Cancer letters · 2026Article
- The Concise Guide to PHARMACOLOGY 2025/26: Catalytic receptors.British journal of pharmacology · 2025Review
- Exploiting collateral sensitivity in the evolution of resistance to tyrosine kinase inhibitors in soft tissue sarcomas.Communications biology · 2025Article
- Metachronous development of L858R and T790M EGFR mutations following ALK inhibitor therapy in stage IV lung adenocarcinoma: a case report.Translational lung cancer research · 2025Article
- In Silico Screening of 1,3,4-Thiadiazole Derivatives as Inhibitors of Vascular Endothelial Growth Factor Receptor-2 (VEGFR-2).Current issues in molecular biology · 2024Article
- Radiotherapy plus temozolomide with or without anlotinib in H3K27M-mutant diffuse midline glioma: A retrospective cohort study.CNS neuroscience & therapeutics · 2024Article
- Tyrphostin A9 attenuates glioblastoma growth by suppressing PYK2/EGFR-ERK signaling pathway.Journal of neuro-oncology · 2023Article
- Predicting Novel Drug Candidates for Pancreatic Neuroendocrine Tumors via Gene Signature Comparison and Connectivity Mapping.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2022Article
- Reciprocal priming between receptor tyrosine kinases at recycling endosomes orchestrates cellular signalling outputs.The EMBO journal · 2021Article
- Review
- Article
- Targeting the Src Pathway Enhances the Efficacy of Selective FGFR Inhibitors in Urothelial Cancers with FGFR3 Alterations.International journal of molecular sciences · 2020Article
- The role of RICTOR amplification in targeted therapy and drug resistance.Molecular medicine (Cambridge, Mass.) · 2020Review
- Degradation of proteins by PROTACs and other strategies.Acta pharmaceutica Sinica. B · 2020Review
- Functional RNAi Screens Define Distinct Protein Kinase Vulnerabilities in EGFR-Dependent HNSCC Cell Lines.Molecular pharmacology · 2019Article
- Semaphorin 3C as a Therapeutic Target in Prostate and Other Cancers.International journal of molecular sciences · 2019Review
- Colony stimulating factor-1 receptor promotes proliferation, migration and invasion in the human nasopharyngeal carcinoma 6-10B cell line via the phosphoinositide 3-kinase/Akt pathway.Oncology letters · 2018Article
- Mechanisms of rapid cancer cell reprogramming initiated by targeted receptor tyrosine kinase inhibitors and inherent therapeutic vulnerabilities.Molecular cancer · 2018Review
- Quantitative phosphoproteomic analysis of acquired cancer drug resistance to pazopanib and dasatinib.Journal of proteomics · 2018Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Studies over the past decade have shown that many cancers have evolved receptor tyrosine kinase (RTK) co-activation as a mechanism to drive tumour progression and limit the lethal effects of therapy. This review summarises the general principles of RTK co-activation and discusses approaches to exploit this phenomenon in cancer therapy and drug discovery. Computational strategies to predict kinase co-dependencies by integrating drug screening data and kinase inhibitor selectivity profiles will also be described. We offer a perspective on the implications of RTK co-activation on tumour heterogeneity and cancer evolution and conclude by surveying emerging computational and experimental approaches that will provide insights into RTK co-activation biology and deliver new developments in effective 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.