Literature DB >> 24846037

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

Mark G Kris1, Bruce E Johnson2, Lynne D Berry3, David J Kwiatkowski4, A John Iafrate5, Ignacio I Wistuba6, Marileila Varella-Garcia7, Wilbur A Franklin7, Samuel L Aronson8, Pei-Fang Su3, Yu Shyr3, D Ross Camidge7, Lecia V Sequist5, Bonnie S Glisson6, Fadlo R Khuri9, Edward B Garon10, William Pao3, Charles Rudin11, Joan Schiller12, Eric B Haura13, Mark Socinski14, Keisuke Shirai15, Heidi Chen3, Giuseppe Giaccone16, Marc Ladanyi1, Kelly Kugler7, John D Minna12, Paul A Bunn7.   

Abstract

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 (<1%); MET amplification, 5 (<1%); NRAS, 5 (<1%); MEK1, 1 (<1%); AKT1, 0. Results were used to select a targeted therapy or trial in 275 of 1007 patients (28%). The median survival was 3.5 years (interquartile range [IQR], 1.96-7.70) for the 260 patients with an oncogenic driver and genotype-directed therapy compared with 2.4 years (IQR, 0.88-6.20) for the 318 patients with any oncogenic driver(s) who did not receive genotype-directed therapy (propensity score-adjusted hazard ratio, 0.69 [95% CI, 0.53-0.9], P = .006). CONCLUSIONS AND RELEVANCE: Actionable drivers were detected in 64% of lung adenocarcinomas. Multiplexed testing aided physicians in selecting therapies. Although individuals with drivers receiving a matched targeted agent lived longer, randomized trials are required to determine if targeting therapy based on oncogenic drivers improves survival. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01014286.

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Year:  2014        PMID: 24846037      PMCID: PMC4163053          DOI: 10.1001/jama.2014.3741

Source DB:  PubMed          Journal:  JAMA        ISSN: 0098-7484            Impact factor:   56.272


  40 in total

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Journal:  Nature       Date:  2007-11-04       Impact factor: 49.962

4.  EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib.

Authors:  William Pao; Vincent Miller; Maureen Zakowski; Jennifer Doherty; Katerina Politi; Inderpal Sarkaria; Bhuvanesh Singh; Robert Heelan; Valerie Rusch; Lucinda Fulton; Elaine Mardis; Doris Kupfer; Richard Wilson; Mark Kris; Harold Varmus
Journal:  Proc Natl Acad Sci U S A       Date:  2004-08-25       Impact factor: 11.205

5.  EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.

Authors:  J Guillermo Paez; Pasi A Jänne; Jeffrey C Lee; Sean Tracy; Heidi Greulich; Stacey Gabriel; Paula Herman; Frederic J Kaye; Neal Lindeman; Titus J Boggon; Katsuhiko Naoki; Hidefumi Sasaki; Yoshitaka Fujii; Michael J Eck; William R Sellers; Bruce E Johnson; Matthew Meyerson
Journal:  Science       Date:  2004-04-29       Impact factor: 47.728

6.  Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib.

Authors:  Thomas J Lynch; Daphne W Bell; Raffaella Sordella; Sarada Gurubhagavatula; Ross A Okimoto; Brian W Brannigan; Patricia L Harris; Sara M Haserlat; Jeffrey G Supko; Frank G Haluska; David N Louis; David C Christiani; Jeff Settleman; Daniel A Haber
Journal:  N Engl J Med       Date:  2004-04-29       Impact factor: 91.245

7.  Integration of molecular profiling into the lung cancer clinic.

Authors:  William Pao; Mark G Kris; A John Iafrate; Marc Ladanyi; Pasi A Jänne; Ignacio I Wistuba; Ryn Miake-Lye; Roy S Herbst; David P Carbone; Bruce E Johnson; Thomas J Lynch
Journal:  Clin Cancer Res       Date:  2009-08-25       Impact factor: 12.531

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10.  Effective use of PI3K and MEK inhibitors to treat mutant Kras G12D and PIK3CA H1047R murine lung cancers.

Authors:  Jeffrey A Engelman; Liang Chen; Xiaohong Tan; Katherine Crosby; Alexander R Guimaraes; Rabi Upadhyay; Michel Maira; Kate McNamara; Samanthi A Perera; Youngchul Song; Lucian R Chirieac; Ramneet Kaur; Angela Lightbown; Jessica Simendinger; Timothy Li; Robert F Padera; Carlos García-Echeverría; Ralph Weissleder; Umar Mahmood; Lewis C Cantley; Kwok-Kin Wong
Journal:  Nat Med       Date:  2008-11-30       Impact factor: 53.440

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Journal:  J Natl Compr Canc Netw       Date:  2014-11       Impact factor: 11.908

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