Drug-resistance mutations in EGFR

NSCLC accounts for 85–90% of all lung cancers and is driven by alterations in oncogenes, such as EGFR. Variable exon 19 deletions in codons 746–753 and the L858R point mutation account for ~90% of all activating EGFR mutations in NSCLC and respond well to the first-generation tyrosine kinase inhibitors (TKIs), gefitinib and erlotinib. GeneTAG has developed a nearly comprehensive set of iDDS probe assays for EGFR mutations that confer resistance or show susceptibility to first-, second-, or third-generation TKIs used in NSCLC. The performance of each probe is shown below. Feel free to let us know if you would like more info regarding drug-resistance and drug-susceptibility profiles.