Cell Line Name：

EGFR L858R-T790M-C797S/BaF3

Host Cell:

Ba/F3

Application:

Anti-proliferation assay and PD assay

Freeze Medium:

90% FBS+10% DMSO

Complete Culture Medium:

Mycoplasma Status:

Negative

EGFR is widely recognized for its importance in cancer. Amplification and mutations have been shown to be driving events in many cancer types. Its role in non-small cell lung cancer, glioblastoma and basal-like breast cancers has spurred many research and drug development efforts. Tyrosine kinase inhibitors have shown efficacy in EGFR amplfied tumors, most notably gefitinib and erlotinib. Mutations in EGFR have been shown to confer resistance to these drugs, particularly the variant T790M, which has been functionally characterized as a resistance marker for both of these drugs. The later generation TKI's have seen some success in treating these resistant cases, and targeted sequencing of the EGFR locus has become a common practice in treatment of non-small cell lung cancer. Overproduction of ligands is another possible mechanism of activation of EGFR. ERBB ligands include EGF, TGF-a, AREG, EPG, BTC, HB-EGF, EPR and NRG1-4 (for detailed information please refer to the respective ligand section). In ligand-activated cancers, Cetuximab appears to be more effective than tyrosine-kinase inhibitors.

1. WB of EGFR-L858R/T790M/C797S expression

Figure 1. WB of EGFR Expression
Lane 1: Negative control
Lane 2: EGFR-WT
Lane 3: EGFR-L858R/T790M
Lane 4: EGFR-L858R/T790M/C797S

2. Sanger sequencing

Figure 2. Sanger Sequencing of EGFR-L858R/T790M/C797S

3. Anti-proliferation assay

Figure 3. Anti-proliferation assay of three reference compounds on the EGFR L858R-T790M-C797S/BaF3 Stable Cell Line.