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Journal conference Vincent T. DeVita, Jr., M.D., and Steven A. Rosenberg, M.D., Ph.D. N Engl J Med 2012;366:2207-14. R2 Seon-Hye Kim, Prof. Sun-kyung Beak Advanced lung adenocarcinoma + EGFR mutation (+) - the first-line erlotinib or gefitinib - high objective response rate & long progression-free survival and overall survival All patients’ treatment eventually fails. - resistance to EGFR tyrosine-kinase inhibitors (TKIs) - characterised by the so-called gatekeeper mutation, T790M Advanced lung adenocarcinoma + EGFR mutation (+) - the first-line erlotinib or gefitinib - high objective response rate & long progression-free survival and overall survival All patients’ treatment eventually fails. - resistance to EGFR tyrosine-kinase inhibitors (TKIs) - characterised by the so-called gatekeeper mutation, T790M Advanced lung adenocarcinoma + EGFR mutation (+) - the first-line erlotinib or gefitinib - high objective response rate & long progression-free survival and overall survival All patients’ treatment eventually fails. - resistance to EGFR tyrosine-kinase inhibitors (TKIs) - characterised by the so-called gatekeeper mutation, T790M Advanced lung adenocarcinoma + EGFR mutation (+) - the first-line erlotinib or gefitinib - high objective response rate & long progression-free survival and overall survival All patients’ treatment eventually fails. - resistance to EGFR tyrosine-kinase inhibitors (TKIs) - characterised by the so-called gatekeeper mutation, T790M Irreversible ErbB-family blocker : Afatinib : M/C mutations, L858R and deletion-19 & the exon 20 gatekeeper T790M mutation. EVALUATION : to assess its efficacy in patients with advanced lung adenoca. with previous treatment failure on EGFR tyrosine kinase inhibitors. Irreversible ErbB-family blocker : Afatinib : M/C mutations, L858R and deletion-19 & the exon 20 gatekeeper T790M mutation. EVALUATION : to assess its efficacy in patients with advanced lung adenoca. with previous treatment failure on EGFR tyrosine kinase inhibitors. 5-yr relative survival rate for all cancers Late 1960s Now 2015 38% 68% 80% Overall rates of death from cancer Late 1960s Now 2015 100% 76% 62% Most of the current declines are the result of the widespread implementation of old technology for diagnosis, prevention, and treatment. However, the clinical application of the fruits of the extra-ordinary molecular revolution is yet to come and cannot be measured with the use of current statistics. The sequencing of the human genome in 2000 has had a profound effect on all of medicine. The cost of sequencing will be much cheaper, putting in the realm of a routine laboratory test. Detected abnormalities will become targets of relatively simple drug therapies, and if the effects mirror what we have seen in recent years with targeted therapy, the ability to prevent or treat cancers in the future will be impressive. The economic and social consequences of converting cancer into a curable or chronic disease will be both gratifying and daunting.