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Prospective Comprehensive Molecular Characterization of Lung Adenocarcinomas for Efficient Patient Matching to Approved and Emerging Therapies
Open accessPublished version of a preprint
Abstract
Tumor genetic testing is standard of care for patients with advanced lung adenocarcinoma, but the fraction of patients who derive clinical benefit remains undefined. Here, we report the experience of 860 patients with metastatic lung adenocarcinoma analyzed prospectively for mutations in >300 cancer-associated genes. Potentially actionable genetic events were stratified into one of four levels based upon published clinical or laboratory evidence that the mutation in question confers increased sensitivity to standard or investigational therapies. Overall, 37.1% (319/860) of patients received a matched therapy guided by their tumor molecular profile. Excluding alterations associated with standard-of-care therapy, 14.4% (69/478) received matched therapy, with a clinical benefit of 52%. Use of matched therapy was strongly influenced by the level of preexistent clinical evidence that the mutation identified predicts for drug response. Analysis of genes mutated significantly more often in tumors without known actionable mutations nominated STK11 and KEAP1 as possible targetable mitogenic drivers. Significance: An increasing number of therapies that target molecular alterations required for tumor maintenance and progression have demonstrated clinical activity in patients with lung adenocarcinoma. The data reported here suggest that broader, early testing for molecular alterations that have not yet been recognized as standard-of-care predictive biomarkers of drug response could accelerate the development of targeted agents for rare mutational events and could result in improved clinical outcomes. Cancer Discov; 7(6); 596–609. ©2017 AACR. See related commentary by Liu et al., p. 555. This article is highlighted in the In This Issue feature, p. 539
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In the citing paper
“Inactivating mutations or loss of STK11/LKB1, which define one of the major genomic sub-groups of KRAS-mutant lung cancers1,19,62, are of particular interest because they are associated with decreased responsiveness to immune checkpoint blockade9,63 and poor overall prognosis64.”
From LKB1 regulates JNK-dependent stress signaling and apoptotic dependency of KRAS-mutant lung cancers (2025) · cites this paper as [62]
Experimental — accuracy not yet measuredIn the citing paper
“KRAS mutations predominate in NSCLCs, accounting for ~78% of all RAS mutations found in such tumours17. The activating missense KRAS mutations that occur in ~25% of NSCLCs19–23 are typically mutually exclusive with other clinically actionable driver mutations, such as those in EGFR, BRAF and ALK24.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [21]
In the citing paper
“Importantly, large-scale profiling studies utilizing either whole exome sequencing or broad targeted sequencing panels in NSCLC tumors have revealed multiple non-random patterns of co-occurring or mutually exclusive mutations, which typically vary depending on the particular oncogenic driver mutation15, 34, 58–62.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [59]
In the citing paper
“Somatic mutations in LKB1 and KEAP1 significantly co-occur with mutant KRAS and with each other in NSCLC15, 59, 63, 91.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [59]
In the citing paper
“Landmark large scale sequencing studies have established a census of major KRAS co-mutations in both early-stage and advanced LUAD15, 34, 59, 62.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [59]
In the citing paper
“Activating mutations in KRAS are the most prevalent oncogenic driver event in both early-stage and metastatic LUAD, occurring in 25–32% of tumors34, 59, 60, 62, 67.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [59]
In the citing paper
“Although EGFR –mutant tumors represent the prototypical oncogene-addicted LUAD subgroup that spearheaded adoption of the single-driver model, the overwhelming majority of EGFR-mutant lung tumors harbor one or more co-mutations, even when the analysis is limited to pre-defined sets of cancer-relevant genes within established panels (FoundationOne, Guardant360, MSK-IMPACT)15, 59, 72, 73.”
From Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy (2019) · cites this paper as [59]
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Cites
PD-1 and PD-L1 Immune Checkpoint Blockade to Treat Breast Cancer
Hartkopf, A. D., Taran, F., Wallwiener, M., Walter, C. B., Krämer, B., Grischke, E., & Brucker, S. Y. (2016) · Breast Care · doi:10.1159/000453569 · Cited by 30,989
Cerami, E., Gao, J., Dogrusoz, U., Gross, B. E., Sumer, S. O., Aksoy, B. A., Jacobsen, A., Byrne, C. J., Heuer, M. L., Larsson, E., et al. (2012) · Cancer Discovery · doi:10.1158/2159-8290.cd-12-0095 · Cited by 17,455
Self-citationIntegrative Analysis of Complex Cancer Genomics and Clinical Profiles Using the cBioPortal
Gao, J., Aksoy, B. A., Dogrusoz, U., Dresdner, G., Gross, B., Sumer, S. O., Sun, Y., Jacobsen, A., Sinha, R., Larsson, E., et al. (2013) · Science Signaling · doi:10.1126/scisignal.2004088 · Cited by 15,160
Self-citationMutational landscape determines sensitivity to PD-1 blockade in non–small cell lung cancer
Rizvi, N. A., Hellmann, M. D., Snyder, A., Kvistborg, P., Makarov, V., Havel, J. J., Lee, W., Yuan, J., Wong, P., Ho, T. S., et al. (2015) · Science · doi:10.1126/science.aaa1348 · Cited by 7,802
Self-citationComprehensive molecular profiling of lung adenocarcinoma
The Cancer Genome Atlas Research Network (2014) · Nature · doi:10.1038/nature13385 · Cited by 5,732
Rosell, R., Carcereny, E., Gervais, R., Vergnenegre, A., Massuti, B., Felip, E., Palmero, R., Garcia-Gomez, R., Pallares, C., Sanchez, J. M., et al. (2012) · The Lancet Oncology · doi:10.1016/s1470-2045(11)70393-x · Cited by 5,489
Crizotinib versus Chemotherapy in Advanced ALK -Positive Lung Cancer
Shaw, A. T., Kim, D.-W., Nakagawa, K., Seto, T., Crinó, L., Ahn, M.-J., De Pas, T., Besse, B., Solomon, B. J., Blackhall, F., et al. (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1214886 · Cited by 3,381
Self-citationFirst-Line Crizotinib versus Chemotherapy in ALK -Positive Lung Cancer
Solomon, B. J., Mok, T., Kim, D.-W., Wu, Y.-L., Nakagawa, K., Mekhail, T., Felip, E., Cappuzzo, F., Paolini, J., Usari, T., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1408440 · Cited by 3,190
Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets (MSK-IMPACT)
Cheng, D. T., Mitchell, T. N., Zehir, A., Shah, R. H., Benayed, R., Syed, A., Chandramohan, R., Liu, Z. Y., Won, H. H., Scott, S. N., et al. (2015) · The Journal of Molecular Diagnostics · doi:10.1016/j.jmoldx.2014.12.006 · Cited by 2,119
Self-citationUsing Multiplexed Assays of Oncogenic Drivers in Lung Cancers to Select Targeted Drugs
Kris, M. G., Johnson, B. E., Berry, L. D., Kwiatkowski, D. J., Iafrate, A. J., Wistuba, I. I., Varella-Garcia, M., Franklin, W. A., Aronson, S. L., Su, P.-F., et al. (2014) · JAMA · doi:10.1001/jama.2014.3741 · Cited by 1,724
Self-citationROS1 Rearrangements Define a Unique Molecular Class of Lung Cancers
Bergethon, K., Shaw, A. T., Ignatius Ou, S.-H., Katayama, R., Lovly, C. M., McDonald, N. T., Massion, P. P., Siwak-Tapp, C., Gonzalez, A., Fang, R., et al. (2012) · Journal of Clinical Oncology · doi:10.1200/jco.2011.35.6345 · Cited by 1,555
Shen, R., & Seshan, V. (2016) · Nucleic Acids Research · doi:10.1093/nar/gkw520 · Cited by 1,263
Dysfunctional KEAP1–NRF2 Interaction in Non-Small-Cell Lung Cancer
Singh, A., Misra, V., Thimmulappa, R. K., Lee, H., Ames, S., Hoque, M. O., Herman, J. G., Baylin, S. B., Sidransky, D., Gabrielson, E., et al. (2006) · PLoS Medicine · doi:10.1371/journal.pmed.0030420 · Cited by 1,060
Barlési, F., Mazières, J., Merlio, J., Debieuvre, D., Mosser, J., Léna, H., Ouafik, L., Besse, B., Rouquette, I., Westeel, V., et al. (2016) · The Lancet · doi:10.1016/s0140-6736(16)00004-0 · Cited by 1,000
Chang, M. T., Asthana, S., Gao, S. P., Lee, B. H., Chapman, J. S., Kandoth, C., Gao, J., Socci, N. D., Solit, D. B., Olshen, A. B., et al. (2016) · Nature Biotechnology · doi:10.1038/nbt.3391 · Cited by 808
Self-citationIntragenic ERBB2 kinase mutations in tumours
Stephens, P., Hunter, C., Bignell, G., Edkins, S., Davies, H., Teague, J., Stevens, C., O'Meara, S., Smith, R., Parker, A., et al. (2004) · Nature · doi:10.1038/431525b · Cited by 802
Brusatol enhances the efficacy of chemotherapy by inhibiting the Nrf2-mediated defense mechanism
Ren, D., Villeneuve, N. F., Jiang, T., Wu, T., Lau, A., Toppin, H. A., & Zhang, D. D. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1014275108 · Cited by 673
Jänne, P. A., Shaw, A. T., Pereira, J. R., Jeannin, G., Vansteenkiste, J., Barrios, C., Franke, F. A., Grinsted, L., Zazulina, V., Smith, P., et al. (2013) · The Lancet Oncology · doi:10.1016/s1470-2045(12)70489-8 · Cited by 655
Yasuda, H., Kobayashi, S., & Costa, D. B. (2012) · The Lancet Oncology · doi:10.1016/s1470-2045(11)70129-2 · Cited by 610
Paik, P. K., Drilon, A. E. D. C., Fan, P., Yu, H. A., Rekhtman, N., Ginsberg, M. S., Borsu, L. A., Schultz, N. D., Berger, M. F., Rudin, C. M., et al. (2015) · Cancer Discovery · doi:10.1158/2159-8290.cd-14-1467 · Cited by 583
Self-citationDrilon, A. E. D. C., Rekhtman, N., Arcila, M. E., Wang, L., Ni, A., Albano, M., van Voorthuysen, M., Somwar, R., Smith, R. S., Montecalvo, J., et al. (2016) · The Lancet Oncology · doi:10.1016/s1470-2045(16)30562-9 · Cited by 494
Self-citationArcila, M. E., Nafa, K., Chaft, J. E., Rekhtman, N., Lau, C., Reva, B. A., Zakowski, M. F., Kris, M. G., & Ladanyi, M. (2013) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-12-0620 · Cited by 473
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Self-citationPlanchard, D., Kim, T. M., Mazieres, J., Quoix, E., Riely, G., Barlesi, F., Souquet, P.-J., Smit, E. F., Groen, H. J. M., Kelly, R. J., et al. (2016) · The Lancet Oncology · doi:10.1016/s1470-2045(16)00077-2 · Cited by 453
Self-citationMeric-Bernstam, F., Brusco, L., Shaw, K., Horombe, C., Kopetz, S., Davies, M. A., Routbort, M., Piha-Paul, S. A., Janku, F., Ueno, N., et al. (2015) · Journal of Clinical Oncology · doi:10.1200/jco.2014.60.4165 · Cited by 424
Development of Therapeutic Combinations Targeting Major Cancer Signaling Pathways
Yap, T. A., Omlin, A. G., & Bono, J. S. D. (2013) · Journal of Clinical Oncology · doi:10.1200/jco.2011.37.6418 · Cited by 335
Kris, M. G., Camidge, D. R., Giaccone, G., Hida, T., Li, B. T., O'Connell, J., Taylor, I., Zhang, H., Arcila, M. E., Goldberg, Z., et al. (2015) · Annals of Oncology · doi:10.1093/annonc/mdv186 · Cited by 334
Self-citationMazières, J., Barlési, F., Filleron, T., Besse, B., Monnet, I., Beau‐Faller, M., Peters, S., Dansin, É., Früh, M., Pless, M., et al. (2015) · Annals of Oncology · doi:10.1093/annonc/mdv573 · Cited by 326
CD74–NRG1 Fusions in Lung Adenocarcinoma
Fernandez‐Cuesta, L., Plenker, D., Osada, H., Sun, R., Menon, R., Leenders, F., Ortiz‐Cuaran, S., Peifer, M., Bos, M. C. A., Daßler, J., et al. (2014) · Cancer Discovery · doi:10.1158/2159-8290.cd-13-0633 · Cited by 295
Mig6 is a negative regulator of EGF receptor–mediated skin morphogenesis and tumor formation
Ferby, I., Reschke, M., Kudlacek, O., Knyazev, P. G., Panté, G., Amann, K., Sommergruber, W., Kraut, N., Ullrich, A., Fässler, R., et al. (2006) · Nature Medicine · doi:10.1038/nm1401 · Cited by 259
Kummar, S., Chen, H. X., Wright, J., Holbeck, S. L., Millin, M. D., Tomaszewski, J. E., Zweibel, J., Collins, J. M., & Doroshow, J. H. (2010) · Nature Reviews Drug Discovery · doi:10.1038/nrd3216 · Cited by 254
Chaft, J. E., Arcila, M. E., Paik, P. K., Lau, C., Riely, G. J., Pietanza, M. C., Zakowski, M. F., Rusch, V. W., Sima, C. S., Ladanyi, M., et al. (2011) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-11-0692 · Cited by 202
Self-citationVansteenkiste, J., Canon, J.-L. R., de Braud, F., Grossi, F., Pas, T. M. D., Gray, J. E., Su, W., Felip, E., Yoshioka, H., Gridelli, C., et al. (2015) · Journal of Thoracic Oncology · doi:10.1097/jto.0000000000000607 · Cited by 163
Luteolin inhibits the Nrf2 signaling pathway and tumor growth in vivo
Chian, S., Thapa, R., Chi, Z., Wang, X. J., & Tang, X. (2014) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2014.04.039 · Cited by 157
Characteristics of Lung Cancers Harboring NRAS Mutations
Ohashi, K., Sequist, L. V. D., Arcila, M. E., Lovly, C. M., Chen, X., Rudin, C. M., Morán, T., Camidge, D. R., Vnencak‐Jones, C. L., Berry, L. D., et al. (2013) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-12-3173 · Cited by 147
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Self-citationClinical characteristics and outcome of patients with lung cancer harboring BRAF mutations
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Gallant, J., Sheehan, J. H., Shaver, T. M., Bailey, M., Lipson, D., Chandramohan, R., Brewer, M. R., York, S. J., Kris, M. G., Pietenpol, J. A., et al. (2015) · Cancer Discovery · doi:10.1158/2159-8290.cd-15-0654 · Cited by 128
Self-citationLee, V. H.-F., Tin, V. P., Choy, T., Lam, K. O., Choi, C., Chung, L.-P., Tsang, J. W. H., Ho, P., Leung, D. K., Ma, E. S. K., et al. (2013) · Journal of Thoracic Oncology · doi:10.1097/jto.0b013e31829f684a · Cited by 123
Oncogenic and sorafenib-sensitive ARAF mutations in lung adenocarcinoma
Imielinski, M. B., Greulich, H. E., Kaplan, B., Araujo, L. H., Amann, J. M., Horn, L., Schiller, J. H., Villalona-Calero, M. A., Meyerson, M. M., & Carbone, D. P. (2014) · Journal of Clinical Investigation · doi:10.1172/jci72763 · Cited by 122
Identification of Recurrent FGFR3–TACC3 Fusion Oncogenes from Lung Adenocarcinoma
Capelletti, M., Dodge, M. E., Ercan, D., Hammerman, P. S., Park, S.-I., Kim, J., Sasaki, H., Jablons, D. M., Lipson, D., Young, L., et al. (2014) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-14-1337 · Cited by 115
Eng, J., Woo, K. M., Sima, C. S., Plodkowski, A., Hellmann, M. D., Chaft, J. E., Kris, M. G., Arcila, M. E., Ladanyi, M., & Drilon, A. (2015) · Journal of Thoracic Oncology · doi:10.1097/jto.0000000000000671 · Cited by 107
Self-citationmTOR Inhibitor Treatment of Pancreatic Cancer in a Patient With Peutz-Jeghers Syndrome
Klümpen, H., Queiroz, K. C. S., Spek, C. A., van Noesel, C. J. M., Brink, H. C., de Leng, W. W. J., de Wilde, R. F., Mathus-Vliegen, E. M. H., Offerhaus, G. J. A., Alleman, M. A., et al. (2010) · Journal of Clinical Oncology · doi:10.1200/jco.2010.32.7825 · Cited by 88
Banno, E., Togashi, Y., Nakamura, Y., Chiba, M., Kobayashi, Y., Hayashi, H., Terashima, M., de Velasco, M. A., Sakai, K., Fujita, Y., et al. (2016) · Cancer Science · doi:10.1111/cas.12980 · Cited by 87
Chen, Z., Feng, J., Saldivar, J.-S., Gu, D., Bockholt, A., & Sommer, S. S. (2008) · Oncogene · doi:10.1038/onc.2008.71 · Cited by 81
Schirosi, L., Nannini, N., Nicoli, D., Cavazza, A., Valli, R., Buti, S., Garagnani, L., Sartori, G., Calabrese, F., Marchetti, A., et al. (2012) · Annals of Oncology · doi:10.1093/annonc/mdr626 · Cited by 75
Maity, T. K., Venugopalan, A., Linnoila, I., Cultraro, C. M., Giannakou, A., Nemati, R., Zhang, X., Webster, J. D., Ritt, D., Ghosal, S., et al. (2015) · Cancer Discovery · doi:10.1158/2159-8290.cd-14-0750 · Cited by 73
Mutation of Lkb1 and p53 Genes Exert a Cooperative Effect on Tumorigenesis
Wei, C., Amos, C. I., Stephens, L. C., Campos, I. M., Deng, J. M., Behringer, R. R., Rashid, A., & Frazier, M. L. (2005) · Cancer Research · doi:10.1158/0008-5472.can-05-0716 · Cited by 66
Locatelli-Sanchez, M., Couraud, S., Arpin, D., Riou, R., Bringuier, P., & Souquet, P.-J. (2013) · Lung · doi:10.1007/s00408-013-9482-4 · Cited by 43
Research works printed but not linked: 2
- OncoKB.org, 2016, Precision Oncology Knowledge Base [Internet]
- Banno, 2016, : 10.1111/.12980, Sensitivities to various EGFR-TKIs of uncommon EGFR mutations L861Q and S768I: what is the optimal EGFR-TKI?, Cancer Sci · DOI
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Metadata
- Authors
- Jordan, E. J., Kim, H. R., Arcila, M. E., Barron, D., Chakravarty, D., Gao, J., Chang, M. T., Ni, A., Kundra, R., Jonsson, P., Jayakumaran, G., Gao, S. P., Johnsen, H. C., Hanrahan, A. J., Zehir, A., Rekhtman, N., Ginsberg, M. S., Li, B. T., Yu, H. A., Paik, P. K., Drilon, A., Hellmann, M. D., Reales, D. N., Benayed, R., Rusch, V. W., Kris, M. G., Chaft, J. E., Baselga, J., Taylor, B. S., Schultz, N., Rudin, C. M., Hyman, D. M., Berger, M. F., Solit, D. B., Ladanyi, M., & Riely, G. J.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- 6Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York.
- 1Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.
- Corresponding author
- Riely, Gregory J.
- ORCID
- Jordan, Emmet J.
- Kim, Hyunjae R.
- Arcila, Maria E.
- Chakravarty, Debyani
- Gao, JianJiong
- Kundra, Ritika
- Jonsson, Philip
- Jayakumaran, Gowtham
- Zehir, Ahmet
- Rekhtman, Natasha
- Ginsberg, Michelle S.
- Li, Bob T.
- Yu, Helena A.
- Paik, Paul K.
- Drilon, Alexander
- Hellmann, Matthew D.
- Reales, Dalicia N.
- Benayed, Ryma
- Rusch, Valerie W.
- Kris, Mark G.
- Chaft, Jamie E.
- Taylor, Barry S.
- Schultz, Nikolaus
- Rudin, Charles M.
- Hyman, David M.
- Berger, Michael F.
- Solit, David B.
- Ladanyi, Marc
- Riely, Gregory J.
- Venue
- Cancer Discovery
- Published
- 2017-06-01
- Volume
- 7
- Issue
- 6
- Pages
- 596-609
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- PMC
- PMC5482929
- OpenAlex
- W2603411876
- Cited by
- 643
- References
- 49
- Citations by year
- 2026: 30 · 2025: 40 · 2024: 65 · 2023: 99 · 2022: 94 · 2021: 101 · 2020: 79 · 2019: 65 · 2018: 55 · 2017: 12
- FWCI
- 47.73
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Discovery (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR002384)
- National Cancer Institute (P30CA008748)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Diagnosis and Treatment
- Keywords
- lung adenocarcinoma, metastatic lung cancer, actionable mutations, targeted therapy, predictive biomarkers, drug response, STK11, Keap1, clinical benefit, molecular profiling
- MeSH terms
- Adenocarcinoma of Lung, Adenocarcinoma, Adolescent, Adult, Aged, Female, Genetic Testing, Humans, Lung Neoplasms, Male, Middle Aged, Mutation, Biomarkers, Tumor, Young Adult, Molecular Targeted Therapy
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