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. 2015 Jan;10(1 Suppl 1):S1-63.
doi: 10.1097/JTO.0000000000000405.

Molecularly targeted therapies in non-small-cell lung cancer annual update 2014

Daniel Morgensztern  1 , Meghan J Campo, Suzanne E Dahlberg, Robert C Doebele, Edward Garon, David E Gerber, Sarah B Goldberg, Peter S Hammerman, Rebecca S Heist, Thomas Hensing, Leora Horn, Suresh S Ramalingam, Charles M Rudin, Ravi Salgia, Lecia V Sequist, Alice T Shaw, George R Simon, Neeta Somaiah, David R Spigel, John Wrangle, David Johnson, Roy S Herbst, Paul Bunn, Ramaswamy Govindan
Affiliations

Molecularly targeted therapies in non-small-cell lung cancer annual update 2014

Daniel Morgensztern et al. J Thorac Oncol. 2015 Jan.

Abstract

There have been significant advances in the understanding of the biology and treatment of non-small-cell lung cancer (NSCLC) during the past few years. A number of molecularly targeted agents are in the clinic or in development for patients with advanced NSCLC. We are beginning to understand the mechanisms of acquired resistance after exposure to tyrosine kinase inhibitors in patients with oncogene addicted NSCLC. The advent of next-generation sequencing has enabled to study comprehensively genomic alterations in lung cancer. Finally, early results from immune checkpoint inhibitors are very encouraging. This review summarizes recent advances in the area of cancer genomics, targeted therapies, and immunotherapy.

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Figures

Figure 1
Figure 1
Potential targetable oncogenes by histology subtype
Figure 2
Figure 2
Chromatin modifying enzymes
Figure 3
Figure 3
ROS1, NTRK1 and RET inhibitors.
Figure 4
Figure 4
KRAS Mutations in NSCLC
Figure 5
Figure 5
Mitotic/Cyclin Inhibitors
Figure 6
Figure 6
PARP inhibition: Mechanism of action (reproduced from Oncology Live, 2013, permission requested)
See this image and copyright information in PMC

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References

    1. Lawrence MS, Stojanov P, Polak P, et al. Mutational heterogeneity in cancer and the search for new cancer-associated genes. Nature. 2013;499:214–218. - PMC - PubMed
    1. Paez JG, Janne PA, Lee JC, et al. EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science (New York, NY) 2004;304:1497–1500. - PubMed
    1. Lynch TJ, Bell DW, Sordella R, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. The New England journal of medicine. 2004;350:2129–2139. - PubMed
    1. Pao W, Miller V, Zakowski M, et al. EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib. Proceedings of the National Academy of Sciences of the United States of America. 2004;101:13306–13311. - PMC - PubMed
    1. Mano H. Non-solid oncogenes in solid tumors: EML4-ALK fusion genes in lung cancer. Cancer science. 2008;99:2349–2355. - PMC - PubMed

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