Signosis/Control (Empty Vector) Ba/F3 Stable Cell Line/EL001NP/1 Ea

Description:

Epidermal growth factor receptor (EGFR) is a cell-surface receptor with intrinsic intracellular protein-tyrosine kinase (TK) activity. LigandbindinginducesEGFRdimerizationandphosphorylation,leadingtotheactivationofEGFRsignalingpathway. Inseveralmalignancies  such  as  non-small  cell  lung  cancer(NSCLC),  EGFR  signaling  is  deregulated  due  tomutations in EGFR, which results in uncontrolledproliferation and migration of tumor cells.EGFRmutationscanleadto“oncogene-addicted”cancers,wherethetumorcellsdependonthemutatedEGFRforcellsurvivalandmalignantphenotype. Oneofthemost  common  EGFR  mutations  foundinhumanpatientsisL858Rsubstitutioninexon21,withintheactivationloopofEGFR.   Patients with this mutationaresensitivetoEGFRtyrosinekinaseinhibitors(TKIs)such as gefitinib or erlotinib, whereas patients withwild type EGFR are not sensitive to TKI.   Anotherclinically relevant mutation associated with acquiredgefitinib and erlotinib resistance is T790M, found inexon 20.   Cells expressing EGFR with both L858Rand  T790M  mutations  are  resistant  to  inducedapoptosis in the presence of gefitinib or erlotinib.   

Data:

Dose-dependentgrowthinhibitionofBaF3cellsharboringEGFRexon20insertionD770-N771insSVDmutation(EL-008),controlBa/F3cellline(EL-001)andEGFRexon20,A767-dupASVmutation(EL-010).Thecellsweretreatedwiththeindicateddoseoferlotinibfor72hoursandcellviabilitywasmeasuredusingSignosisCVCreagent.