| Abstract: |
Thoracic oncologists traditionally have made treatment decisions based upon tumor histology, distinguishing non-small cell lung cancer (NSCLC) from small cell lung cancer (SCLC). However, recent data has revealed that at least one histological subtype of NSCLC, lung adenocarcinoma comprises multiple molecularly distinct diseases. Lung adenocarcinoma subsets now can be defined by specific 'driver' mutations in genes encoding components of the EGFR signaling pathway. Importantly, these mutations have implications regarding targeted therapy. Here, we focus on EGFR mutant NSCLC - a prime example of a clinically relevant molecular subset of lung cancer, with defined mechanisms of drug sensitivity, primary drug resistance, and acquired resistance to EGFR tyrosine kinase inhibitors. Efforts are now being made to overcome mechanisms of acquired resistance. These findings illustrate how knowledge about the genetic drivers of tumors can lead to rational targeted therapy for individual patients. © 2012 Springer-Verlag Berlin Heidelberg. |
| Keywords: |
cancer chemotherapy; treatment response; unclassified drug; overall survival; histopathology; erlotinib; placebo; drug withdrawal; nonhuman; drug targeting; paclitaxel; cancer patient; drug megadose; molecular genetics; antineoplastic agent; protein domain; gastrointestinal stromal tumor; imatinib; carboplatin; unindexed drug; protein targeting; lung non small cell cancer; epidermal growth factor receptor; drug potency; chemosensitivity; dasatinib; chronic myeloid leukemia; cancer resistance; docetaxel; temsirolimus; lung adenocarcinoma; drug mechanism; gefitinib; heat shock protein 90 inhibitor; egfr gene; drug substitution; drug treatment failure; phosphotransferase; everolimus; rapamycin; mutant; epidermal growth factor receptor kinase inhibitor; neratinib; xl 647; 1 (1 cyano 1 methylethyl) 3 methyl 8 (3 quinolinyl)imidazo[4,5 c]quinolin 2(1h,3h) one; afatinib; dacomitinib; 8 [4 (1 aminocyclobutyl)phenyl] 9 phenyl 1,2,4 triazolo[3,4 f][1,6]naphthyridin 3(2h) one; xl 147; bgt 226; bms 690514; pictilisib; triciribine phosphate; xl 418; xl 765; hypereosinophilic syndrome
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