EGF receptor mutations in lung cancer: from humans to mice and maybe back to humans.

Arteaga CL
Cancer Cell. 2006 9 (6): 421-3

PMID: 16766261 · DOI:10.1016/j.ccr.2006.05.014

Deletions in exon 19 and nucleotide substitutions in exon 21 are the most common mutations of the EGFR (ErbB1) in NSCLC. These mutations endow the receptor with constitutive kinase activity. Most tumors expressing these mutants respond well to EGFR tyrosine kinase inhibitors, suggesting that they are dependent on mutant EGFR signaling. Two groups developed transgenic mice in which expression of these mutants is temporally induced in mouse lung. Mice expressing EGFR mutants develop bronchioloalveolar cancer and lung adenocarcinoma, which are highly sensitive to EGFR inhibitors. These mouse models provide important opportunities for studying the biology of NSCLC and the refinement of anti-EGFR therapies.

MeSH Terms (20)

Adenocarcinoma, Bronchiolo-Alveolar Animals Antibodies, Monoclonal Antibodies, Monoclonal, Humanized Antineoplastic Agents Carcinoma, Non-Small-Cell Lung Cetuximab Doxycycline ErbB Receptors Erlotinib Hydrochloride Exons Humans Lung Neoplasms Mice Mice, Transgenic Mutation Protein Kinase Inhibitors Quinazolines Quinolines Signal Transduction

Connections (1)

This publication is referenced by other Labnodes entities:

Links