Using multiplexed assays of oncogenic drivers in lung cancers to select targeted drugs

Mark G. Kris, Bruce E. Johnson, Lynne D. Berry, David J. Kwiatkowski, A. John Iafrate, Ignacio I. Wistuba, Marileila Varella-Garcia, Wilbur A. Franklin, Samuel L. Aronson, Pei Fang Su, Yu Shyr, D. Ross Camidge, Lecia V. Sequist, Bonnie S. Glisson, Fadlo R. Khuri, Edward B. Garon, William Pao, Charles Rudin, Joan Schiller, Eric B. HauraMark Socinski, Keisuke Shirai, Heidi Chen, Giuseppe Giaccone, Marc Ladanyi, Kelly Kugler, John D. Minna, Paul A. Bunn

Research output: Contribution to journalArticlepeer-review

966 Scopus citations


IMPORTANCE: Targeting oncogenic drivers (genomic alterations critical to cancer development and maintenance) has transformed the care of patients with lung adenocarcinomas. The Lung Cancer Mutation Consortium was formed to perform multiplexed assays testing adenocarcinomas of the lung for drivers in 10 genes to enable clinicians to select targeted treatments and enroll patients into clinical trials. OBJECTIVES: To determine the frequency of oncogenic drivers in patients with lung adenocarcinomas and to use the data to select treatments targeting the identified driver(s) and measure survival. DESIGN, SETTING, AND PARTICIPANTS: From 2009 through 2012, 14 sites in the United States enrolled patients with metastatic lung adenocarcinomas and a performance status of 0 through 2 and tested their tumors for 10 drivers. Information was collected on patients, therapies, and survival. INTERVENTIONS: Tumors were tested for 10 oncogenic drivers, and results were used to select matched targeted therapies. MAIN OUTCOMES AND MEASURES: Determination of the frequency of oncogenic drivers, the proportion of patients treated with genotype-directed therapy, and survival. RESULTS: From 2009 through 2012, tumors from 1007 patients were tested for at least 1 gene and 733 for 10 genes (patients with full genotyping). An oncogenic driver was found in 466 of 733 patients (64%). Among these 733 tumors, 182 tumors (25%) had the KRAS driver; sensitizing EGFR, 122 (17%); ALK rearrangements, 57 (8%); other EGFR, 29 (4%); 2 or more genes, 24 (3%); ERBB2 (formerly HER2), 19 (3%); BRAF, 16 (2%); PIK3CA, 6 (

Original languageEnglish (US)
Pages (from-to)1998-2006
Number of pages9
JournalJournal of the American Medical Association
Issue number19
StatePublished - 2014

ASJC Scopus subject areas

  • Medicine(all)


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