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| Title / Description | Microarray study to understand acquired resistance to EGFR-targeted therapy in lung cancer |
| Accession | GSE38310 |
| Summary | Activating mutations of EGFR have been characterized as important mechanisms for carcinogenesis in a subset of EGFR-dependent non-small cell lung cancers (NSCLC). EGFR tyrosine kinase inhibitors (TKI), such as erlotinib and gefitinib, have dramatic clinical effects on EGFR-addicted lung cancers and are used as first-line therapy for EGFR-mutant tumors. However, eventually all tumors acquire secondary resistance to the drugs and progress. We established a model to better understand mechanisms of acquired resistance. NCI- HCC827 cells are EGFR-mutant and highly erlotinib-sensitive. In this study we exposed HCC827 cells to increasing concentrations of erlotinib and two highly erlotinib-resistant subclones were developed (ER3 and T15-2). In these subclones no acquired alterations of EGFR or MET were found. We hereby performed a gene expression microarray studies to understand changes that might explain mechanisms of resistance. Through these studies we demonstrated in one resistant clone (ER3) overexpression of AXL, a tyrosine kinase implicated in imatinib and lapatinib resistance. |
| Organism | Homo sapiens |
| Platform | GPL6947 |
| Normalized | False |
| Parsed SOFT file |
| Differential expression method | Characteristic Direction |
| Cutoff | 500 |
| Cell_type | HCC827 |
| Drug_id | DB00530 |
| Drug_name | Erlotinib - 12hr |
| Organism | Human |
| Principal Component Analysis | |
| Hierarchical clustering |
| Gene lists | Enrichr | L1000CDS2 | PAEA | Crowdsourcing | |
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