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ModelsIto2019 - gefitnib resistance of lung adenocarcinoma caused by MET amplification
The model is based on publication: Mathematical analysis of gefitinib resistance of lung adenocarcinoma caused by MET amplification Abstract: Gefitinib, one of the tyrosine kinase inhibitors of epidermal growth factor receptor (EGFR), is effective for treating lung adenocarcinoma harboring EGFR mut...
2024-09-02 | BIOMD0000000827 | BioModels
TranscriptomicsTranscription profiling by array of human wild type and gefitinib-resistant A431 cancer cells
A431 wild-type (wt) cancer cell line is sensitive to treatment with EGFR tyrosine kinase inhibitors (TKIs). By culturing it chronically under gefitinib, it eventually becomes resistant (A431_GR cell). We know of a few proteins involved in this mechanism of drug resistance, but a cDNA exprssion array...
ORGANISM(S): Homo sapiens 
2008-04-06 | E-GEOD-10696 | biostudies-arrayexpress
ProteomicsExosomal Proteomics Reveals Fatty Acid Metabolism Linked to Gefitinib Resistance in Non-Small Cell Lung Cancer
Extracellular vesicles (EVs) serve as critical mediators of intercellular communication, facilitating drug resistance in tumor microenvironments by transferring bioactive components like proteins. Despite their potential role in non-small cell lung cancer (NSCLC), systematic investigations into exos...
ORGANISM(S): Homo sapiens (Human) 
2025-12-29 | PXD068676 | Pride
Nsclc Proteomics Exosomes Gefitinib resistance Fatty acid metabolism 
TranscriptomicsGenome-wide analysis of gefitinib short-term resistance gene expression in the NSCLC cell line HCC827 in co-culture
Analysis of gefitinib short-term resistance at gene expression level. The hyposthesis tested in the present study was that short-term resistance towards gefitinib in NSCLC cells influences pathways that associates with resistance towards EGFR-TKI treatment. Results provide important information of t...
ORGANISM(S): Homo sapiens 
2016-07-01 | E-GEOD-75307 | biostudies-arrayexpress
TranscriptomicsGenome-wide analysis of gefitinib short-term resistance gene expression in the NSCLC cell line PC9 in co-culture
Analysis of gefitinib short-term resistance at gene expression level. The hyposthesis tested in the present study was that short-term resistance towards gefitinib in NSCLC cells influences pathways that associates with resistance towards EGFR-TKI treatment. Results provide important information of t...
ORGANISM(S): Homo sapiens 
2016-07-01 | E-GEOD-75308 | biostudies-arrayexpress
TranscriptomicsTime-course gene expression profiles of gefitinib-sensitive or -resistant lung adenocarcinoma cells stimulated with EGF, in the presence or absence of gefitinib, EGF receptor tyrosine kinase-specific inhibitor
Gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), induces substantial clinical responses for non-small cell lung cancer (NSCLC) cells harboring EGFR activating mutations, but most of them invariably develop resistance. By generating a gefitinib resistance (PC9GR)...
ORGANISM(S): Homo sapiens 
2014-01-01 | E-GEOD-34228 | biostudies-arrayexpress
TranscriptomicsmiR-134/487b/655 Cluster regulates TGF-M-NM-2-induced epithelial-mesenchymal transition and drug resistance to Gefitinib by targeting MAGI2 in lung adenocarcinoma cells.
Epithelial-mesenchymal transition (EMT) has recently been recognized as a key element of cell invasion, migration, metastasis, and drug resistance in several types of cancer, including non-small cell lung cancer (NSCLC). Our aim was to clarify microRNA (miRNA) -related mechanisms underlying EMT foll...
ORGANISM(S): Homo sapiens 
2013-10-30 | E-GEOD-51828 | biostudies-arrayexpress
TranscriptomicsNSCLC cells treated with Gefitinib
About 10% of all NSCLC patients respond to gefitnib treatment and all of these patients will acquire resistance to the EGFR TKI. We used microarray to look at global gene expression changes in untreated cells vs gefitinib treated cells to identify key characters for the acquisition of resistance. NS...
ORGANISM(S): Homo sapiens 
2011-01-27 | E-GEOD-23206 | biostudies-arrayexpress
TranscriptomicsA mechanism of resistance to gefitinib mediated by cellular reprogramming and the acquisition of an FGF2-FGFR1 autocrine growth loop
Despite initial and often dramatic responses of epidermal growth factor receptor (EGFR)-addicted lung tumors to the EGFR-specific tyrosine kinase inhibitors (TKIs), gefitinib and erlotinib, nearly all develop resistance and relapse. To explore novel mechanisms mediating acquired resistance, we emplo...
ORGANISM(S): Homo sapiens 
2016-03-29 | E-GEOD-79688 | biostudies-arrayexpress
GenomicsCompound kushen injection and YFSJ reduce gefitinib resistance in gefitinib resistant lung cancer cell lines
Compound kushen injection and YFSJ reduce gefitinib resistance in gefitinib resistant lung cancer cell lines
PRJNA518027 | ENA
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