ArticlePloS one2012
Modeling of tumor progression in NSCLC and intrinsic resistance to TKI in loss of PTEN expression.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
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- Uncertainty quantified discovery of chemical reaction systems via Bayesian scientific machine learning.Frontiers in systems biology · 2024Article
- Research progress on the therapeutic effect and mechanism of metformin for lung cancer (Review).Oncology reports · 2023Review
- Ethacrynic Acid Enhances the Antitumor Effects of Afatinib in EGFR/T790M-Mutated NSCLC by Inhibiting WNT/Beta-Catenin Pathway Activation.Disease markers · 2021Article
- Concurrent Genetic Alterations and Other Biomarkers Predict Treatment Efficacy of EGFR-TKIs in EGFR-Mutant Non-Small Cell Lung Cancer: A Review.Frontiers in oncology · 2020Review
- Identification of genetic alterations associated with primary resistance to EGFR-TKIs in advanced non-small-cell lung cancer patients with EGFR sensitive mutations.Cancer communications (London, England) · 2019Article
- ModelBricks-modules for reproducible modeling improving model annotation and provenance.NPJ systems biology and applications · 2019Review
- Transglutaminase 2 induces intrinsic EGFR-TKI resistance in NSCLC harboring EGFR sensitive mutations.American journal of cancer research · 2019Article
- Novel approaches against epidermal growth factor receptor tyrosine kinase inhibitor resistance.Oncotarget · 2018Review
- Tamoxifen-Induced Apoptosis of MCF-7 Cells via GPR30/PI3K/MAPKs Interactions: Verification by ODE Modeling and RNA Sequencing.Frontiers in physiology · 2018Article
- Dynamic modeling of folliculogenesis signaling pathways in the presence of miRNAs expression.Journal of ovarian research · 2017Article
- Activation of an AKT/FOXM1/STMN1 pathway drives resistance to tyrosine kinase inhibitors in lung cancer.British journal of cancer · 2017Article
- Extracellular region of epidermal growth factor receptor: a potential target for anti-EGFR drug discovery.Oncogene · 2017Review
- Small activating ribonucleic acid reverses tyrosine kinase inhibitor resistance in epidermal growth factor receptor-mutant lung cancer by increasing the expression of phosphatase and tensin homolog.Thoracic cancer · 2016Article
- Fisetin, a dietary phytochemical, overcomes Erlotinib-resistance of lung adenocarcinoma cells through inhibition of MAPK and AKT pathways.American journal of translational research · 2016Article
- Intrinsic resistance to EGFR tyrosine kinase inhibitors in advanced non-small-cell lung cancer with activating EGFR mutations.OncoTargets and therapy · 2016Review
- Mechanisms of resistance to EGFR tyrosine kinase inhibitors.Acta pharmaceutica Sinica. B · 2015Review
- An integrated genome-wide approach to discover deregulated microRNAs in non-small cell lung cancer: Clinical significance of miR-23b-3p deregulation.Scientific reports · 2015Article
- Quantitative and logic modelling of molecular and gene networks.Nature reviews. Genetics · 2015Review
- BioModels: Content, Features, Functionality, and Use.CPT: pharmacometrics & systems pharmacology · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EGFR signaling plays a very important role in NSCLC. It activates Ras/ERK, PI3K/Akt and STAT activation pathways. These are the main pathways for cell proliferation and survival. We have developed two mathematical models to relate to the different EGFR signaling in NSCLC and normal cells in the presence or absence of EGFR and PTEN mutations. The dynamics of downstream signaling pathways vary in the disease state and activation of some factors can be indicative of drug resistance. Our simulation denotes the effect of EGFR mutations and increased expression of certain factors in NSCLC EGFR signaling on each of the three pathways where levels of pERK, pSTAT and pAkt are increased. Over activation of ERK, Akt and STAT3 which are the main cell proliferation and survival factors act as promoting factors for tumor progression in NSCLC. In case of loss of PTEN, Akt activity level is considerably increased. Our simulation results show that in the presence of erlotinib, downstream factors i.e. pAkt, pSTAT3 and pERK are inhibited. However, in case of loss of PTEN expression in the presence of erlotinib, pAkt level would not decrease which demonstrates that these cells are resistant to erlotinib.
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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.