Product Name Catalog # Price (NP)**   Qty
EGFR (Del19-T790M) stably expressing BaF3 stable cell line EL-014-NP $1,200
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  • ** Non Profit (NP) price is for academic, non profit organizations and institutes

Epidermal growth factor receptor (EGFR) is a cell-surface receptor with intrinsic intracellular protein-tyrosine kinase (TK) activity. Ligand binding induces EGFR dimerization and phosphorylation, leading to the activation of EGFR signaling pathway. In several malignancies such as non-small cell lung cancer (NSCLC), EGFR signaling is deregulated due to mutations in EGFR, which results in uncontrolled proliferation and migration of tumor cells. EGFR mutations can lead to “oncogene-addicted” cancers, where the tumor cells depend on the mutated EGFR for cell survival and malignant phenotype.  One of the most common EGFR mutations found in human patients is L858R substitution in exon 21, within the activation loop of EGFR. Patients with this mutation are sensitive to EGFR tyrosine kinase inhibitors (TKIs) such as gefitinib or erlotinib, whereas patients with wild type EGFR are not sensitive to TKI. Another clinically relevant mutation associated with acquired gefitinib and erlotinib resistance is T790M, found in exon 20. Cells expressing EGFR with both L858R and T790M mutations are resistant to induced apoptosis in the presence of gefitinib or erlotinib. 


We offer EL-014, a BaF3 stable cell line expressing both EGFR (E19del) and T790M. The EGFR exon 19 mutation is an 11-18 bp in-frame deletion around the ATP-binding site encoded in exon 19 of the EGFR gene, observed in ~15-20% of lung cancer patients. The EGFR T790M mutation arises from the nucleotide change c.2369C>T in exon 20, resulting in an amino acid substitution of the threonine (T) at position 790 by a methionine (M). This cell line can be used to study the molecular mechanism underlying susceptibility of tumors to the drugs (i.e. gefitinib and erlotinib) as well as screening and validating new TKIs. 




Dose-dependent growth inhibition of BaF3 cells harboring EGFR Del19 (EL-011), EGFR Ins19 (EL-009) and representative Erlotinib resistant cell line, EGFR Del19-T790M (EL-014). The cells were treated with the indicated dose of erlotinib for 24 hours and cells viability was measured using Signosis CVC reagent. EGFR Del19 stably expressing BaF3 cells (EL-011) remains 14-fold more sensitive to TKI erlotinib (IC50=0.34) than its resistance derivative EGFR Del19-T790M stably expressing BaF3 cells (EL-014) (IC50=4.9).



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