title: Shades of T790M: Intratumor Heterogeneity in EGFR-Mutant Lung Cancer.
abstract: In the setting of recent exciting clinical results and numerous ongoing trials, Piotrowska and colleagues explore mechanisms of acquired resistance to the mutant-specific EGFR inhibitor rociletinib, and demonstrate that loss of T790M, EGFR amplification, and small-cell transformation are all clinically relevant mechanisms of drug resistance. The authors provide a new paradigm for using quantitative assessment of the EGFR T790M:activation mutation allele frequency ratio to prognosticate responses to rociletinib and also demonstrate that plasma-based assessments of circulating tumor DNA can be used to monitor drug response and the emergence of drug resistance.
authors.affiliation: Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee. Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
authors.forename: Eiki
authors.initials: E
authors.lastname: Ichihara
authors.affiliation: Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee. Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee. Department of Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee. christine.lovly@vanderbilt.edu.
authors.forename: Christine M
authors.initials: CM
authors.lastname: Lovly
mesh_terms: D000178:Acrylamides / Q000008:administration & dosage*; D019008:Drug Resistance, Neoplasm; D066246:ErbB Receptors / Q000235:genetics*; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy*; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage*; D011743:Pyrimidines / Q000008:administration & dosage*; D055752:Small Cell Lung Carcinoma / Q000188:drug therapy*
chemical_list: D000178:Acrylamides; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D066246:ErbB Receptors