Description(s):
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-003, a Ba/F3 stable cell line expressing EGFR L858R. The EGFR L858R mutation arises from the nucleotide change c.2573T>G in exon 21, resulting in an amino acid substitution of the leucine (L) at position 858 by an arginine (R). 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.