Oncogenic transformation by inhibitor-sensitive and resistant EGFR mutants

Background
 
Somatic mutations in the kinase domain of the epidermal growth factor receptor tyrosine kinase gene EGFR are common in lung adenocarcinoma. The presence of mutations correlates with tumor sensitivity to the EGFR inhibitors erlotinib and gefitinib, but the transforming potential of specific mutations and their relationship to drug sensitivity have not been described.
 
Methods and Findings
 
Here, we demonstrate that EGFR active site mutants are oncogenic. Mutant EGFR can transform both fibroblasts and lung epithelial cells in the absence of exogenous epidermal growth factor, as evidenced by anchorage-independent growth, focus formation, and tumor formation in immunocompromised mice. Transformation is associated with constitutive autophosphorylation of EGFR, Shc phosphorylation, and STAT pathway activation. Whereas transformation by most EGFR mutants confers on cells sensitivity to erlotinib and gefitinib, transformation by an exon 20 insertion makes cells resistant to these..., , , # Data from: Oncogenic transformation by inhibitor-sensitive and resistant EGFR mutants

[https://doi.org/10.5061/dryad.nvx0k6f1f](https://doi.org/10.5061/dryad.nvx0k6f1f)

## Description of the data and file structure

These representative photos are fields from a set of soft agar assay plates in which NIH-3T3 cells ectopically expressing wild-type or mutant EGFR are suspended in soft agar to quantify oncogenic potential and measure response to EGFR inhibitors.  Because wild-type EGFR expressing cells are not oncogenically transformed, EGF has been added to stimulate EGFR signaling and soft agar colony formation in order to measure inhibitor response.  This experiment is an independent validation of the conclusions in the PLoS Medicine paper (doi [10.1371/journal.pmed.0020313](https://doi.org/10.1371/journal.pmed.0020313) ), for which the raw image data no longer exist.  This experiment was performed within a few months of the published experiment in 2005.

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