title: Paths of resistance to EGFR inhibitors: is NF enough?
abstract: Although the majority of patients with EGFR-mutant lung cancer respond well to EGF receptor (EGFR) tyrosine kinase inhibitors (TKI), all patients eventually develop resistance. The mechanism of acquired resistance is still unknown for a considerable subset of cases. This study reveals the NF1 tumor suppressor gene as a new mediator of resistance to EGFR TKIs and provides a mechanistic rationale for developing combination therapies.
authors.affiliation: 1Genetics Division, Department of Medicine, Brigham and Women's Hospital; 2Harvard Medical School; and 3Ludwig Center at Dana-Farber/Harvard Cancer Center, Boston, Massachusetts.
authors.forename: Ophélia
authors.initials: O
authors.lastname: Maertens
authors.forename: Karen
authors.initials: K
authors.lastname: Cichowski
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D019008:Drug Resistance, Neoplasm; D066246:ErbB Receptors / Q000037:antagonists & inhibitors / Q000235:genetics; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000235:genetics; D009154:Mutation; D025542:Neurofibromin 1 / Q000235:genetics*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D000970:Antineoplastic Agents; D025542:Neurofibromin 1; D047428:Protein Kinase Inhibitors; D066246:ErbB Receptors