ReviewAmerican journal of cancer research2014
Redundant kinase activation and resistance of EGFR-tyrosine kinase inhibitors.
Review in American journal of cancer research, 2014. 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, 38 citations in OpenAlex.
- A phase II study of tarloxotinib (a hypoxia activated prodrug of a pan-erb tyrosine kinase inhibitor) in patients with recurrent or metastatic squamous cell carcinoma of the head and neck or skin.Investigational new drugs · 2022Trial
- Multi-Faceted Role of Luteolin in Cancer Metastasis: EMT, Angiogenesis, ECM Degradation and Apoptosis.International journal of molecular sciences · 2023Review
- Review
- TDO2 overexpression correlates with poor prognosis, cancer stemness, and resistance to cetuximab in bladder cancer.Cancer reports (Hoboken, N.J.) · 2021Article
- Signaling Pathways in Cancer: Therapeutic Targets, Combinatorial Treatments, and New Developments.Cells · 2021Review
- FGF Signalling in the Self-Renewal of Colon Cancer Organoids.Scientific reports · 2019Article
- Pin1 inhibition potently suppresses gastric cancer growth and blocks PI3K/AKT and Wnt/β-catenin oncogenic pathways.Molecular carcinogenesis · 2019Article
- Evaluation of EGFR mutations in NSCLC with highly sensitive droplet digital PCR assays.Molecular medicine reports · 2019Article
- Lenvatinib, a molecule with versatile application: from preclinical evidence to future development in anti-cancer treatment.Cancer management and research · 2019Review
- NOTCH3 inactivation increases triple negative breast cancer sensitivity to gefitinib by promoting EGFR tyrosine dephosphorylation and its intracellular arrest.Oncogenesis · 2018Article
- Synergistic potentiation of the anti-metastatic effect of anti EGFR mAb by its combination with immunotherapies targeting the ganglioside NGcGM3.Oncotarget · 2018Article
- Receptor tyrosine kinases (RTKs) in breast cancer: signaling, therapeutic implications and challenges.Molecular cancer · 2018Review
- Novel targeted therapies and immunotherapy for advanced thyroid cancers.Molecular cancer · 2018Review
- AKT inhibitor MK-2206 sensitizes breast cancer cells to MLN4924, a first-in-class NEDD8-activating enzyme (NAE) inhibitor.Cell cycle (Georgetown, Tex.) · 2018Article
- Identification of microRNAs involved in gefitinib resistance of non-small-cell lung cancer through the insulin-like growth factor receptor 1 signaling pathway.Experimental and therapeutic medicine · 2017Article
- Urokinase-type plasminogen activator receptor (uPAR) expression enhances invasion and metastasis in RAS mutated tumors.Scientific reports · 2017Article
- Review
- Kidney Fibrosis: Origins and Interventions.Transplantation · 2017Review
- Bayesian model of signal rewiring reveals mechanisms of gene dysregulation in acquired drug resistance in breast cancer.PloS one · 2017Article
- Atypical skin reaction in a patient treated with gefitinib for advanced lung cancer: A case report and review of the literature.Experimental and therapeutic medicine · 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) have shown dramatic effects against that tumors harboring EGFR activating mutations in the EGFR intracytoplasmic tyrosine kinase domain and resulted in cell apoptosis. Unfortunately, a number of patients ultimately developed resistance by multiple mechanisms. Thus, elucidation of the mechanism of resistance to EGFR-TKIs can provide strategies for blocking or reversing the situation. Recent studies suggested that redundant kinase activation plays pivotal roles in escaping from the effects of EGFR-TKIs. Herein, we aimed to characterize several molecular events involved in the resistance to EGFR-TKIs mediated by redundant kinase activation.
Indexed as
Identifiers
25520855PMC4266699W152279435What Socratic 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 Socratic graph.