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 the 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 the 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.
EL-001 is a stable cell line established with an empty vector as a control for three stably expressing  HA-tagged  EGFR  Ba/F3  cell lines; WT   EGFR,   L858R EGFR mutant, L858R/T790M EGFR double mutant.  These cell lines can be used to study the molecular mechanism underlying the susceptibility of tumors to the drugs (i.e. gefitinib and erlotinib) as well as screening and validating new TKIs.