Mapping the Hallmarks of Lung Adenocarcinoma with Massively Parallel Sequencing
Open accessAbstract
Lung adenocarcinoma, the most common subtype of non-small cell lung cancer, is responsible for more than 500,000 deaths per year worldwide. Here, we report exome and genome sequences of 183 lung adenocarcinoma tumor/normal DNA pairs. These analyses revealed a mean exonic somatic mutation rate of 12.0 events/megabase and identified the majority of genes previously reported as significantly mutated in lung adenocarcinoma. In addition, we identified statistically recurrent somatic mutations in the splicing factor gene U2AF1 and truncating mutations affecting RBM10 and ARID1A. Analysis of nucleotide context-specific mutation signatures grouped the sample set into distinct clusters that correlated with smoking history and alterations of reported lung adenocarcinoma genes. Whole-genome sequence analysis revealed frequent structural rearrangements, including in-frame exonic alterations within EGFR and SIK2 kinases. The candidate genes identified in this study are attractive targets for biological characterization and therapeutic targeting of lung adenocarcinoma.
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KRAS mutations account for about 78% of RAS mutations in NSCLC, and activating missense KRAS mutations occur in about 25% of NSCLCs, usually mutually exclusive with other actionable drivers such as EGFR, BRAF and ALK.
“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 [23]
Large-scale profiling studies in NSCLC have revealed multiple non-random patterns of co-occurring or mutually exclusive mutations, which typically vary depending on the particular oncogenic driver mutation.
“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 [62]
Landmark large scale sequencing studies have established a census of major KRAS co-mutations in both early-stage and advanced LUAD.
“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 [62]
Activating mutations in KRAS are the most prevalent oncogenic driver event in both early-stage and metastatic LUAD, occurring in 25-32% of tumors.
“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 [62]
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Inferring tumour purity and stromal and immune cell admixture from expression data
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Self-citationSignatures of mutational processes in human cancer
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Mutational landscape determines sensitivity to PD-1 blockade in non–small cell lung cancer
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Comprehensive molecular profiling of lung adenocarcinoma
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Self-citationThe Somatic Genomic Landscape of Glioblastoma
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“, 2013), lung adenocarcinoma (Imielinski et al., 2012), and melanoma (Berger et al.”
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“We ask: (1) Can large-scale genomic analysis across tumor types reliably identify all known cancer genes? (2) Will it reveal many new candidate cancer genes? (3) How far do we stand from having a complete catalog of cancer genes – at least those of intermediate frequency? We used rigorous statistical methods to enumer…”
BackgroundMethodInfluentialSelf-citationTracking the Evolution of Non–Small-Cell Lung Cancer
Jamal-Hanjani, M., Wilson, G. A., McGranahan, N., Birkbak, N. J., Watkins, T. B. K., Veeriah, S., Shafi, S., Johnson, D. H., Mitter, R., Rosenthal, R., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1616288 · Cited by 2,349 · see citing works
Prospective Derivation of a Living Organoid Biobank of Colorectal Cancer Patients
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Self-citationComprehensive genomic profiles of small cell lung cancer
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Self-citationAn ultrasensitive method for quantitating circulating tumor DNA with broad patient coverage
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The KEAP1-NRF2 system: a thiol-based sensor-effector apparatus for maintaining redox homeostasis
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Non-small-cell lung cancers: a heterogeneous set of diseases
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Self-citationHigh burden and pervasive positive selection of somatic mutations in normal human skin
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Pan-cancer patterns of somatic copy number alteration
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Self-citationHighly Recurrent <i>TERT</i> Promoter Mutations in Human Melanoma
Huang, F. W., Hodis, E., Xu, M. J., Kryukov, G. V., Chin, L., & Garraway, L. A. (2013) · Science · doi:10.1126/science.1229259 · Cited by 1,816 · see citing works
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 · see citing works
Self-citation<i>STK11/LKB1</i> Mutations and PD-1 Inhibitor Resistance in <i>KRAS</i> -Mutant Lung Adenocarcinoma
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“KL KP K-only 54(0) 56(0) 64(0) 25(5) 36(2) 45(4) 10(12) 19(14) 27(18) 4(16) 4(26) 4(34) 2(17) 1(29) 1(37) 1(18) 1(29) 1(37) 1(18) 1(29) 1(37) 0(19) 1(29) 0(38) 0(19) 0(30) 0(38) KL KRASSTK11”
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Lessons from the Cancer Genome
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Self-citationMechanisms and Regulation of Alternative Pre-mRNA Splicing
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Activation of the PD-1 Pathway Contributes to Immune Escape in EGFR-Driven Lung Tumors
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Self-citationDistinct patterns of somatic genome alterations in lung adenocarcinomas and squamous cell carcinomas
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Self-citationThe genetic landscape of high-risk neuroblastoma
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Self-citationRNA-binding proteins in human genetic disease
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Whole-exome sequencing of pancreatic cancer defines genetic diversity and therapeutic targets
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Spatial and temporal diversity in genomic instability processes defines lung cancer evolution
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Mutational signatures associated with tobacco smoking in human cancer
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Identification of genomic alterations in oesophageal squamous cell cancer
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Co-occurring genomic alterations in non-small-cell lung cancer biology and therapy
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Understanding and targeting resistance mechanisms in NSCLC
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Self-citationInterplay between the Cancer Genome and Epigenome
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Epigenetic modulators, modifiers and mediators in cancer aetiology and progression
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Self-citationPan-cancer analysis of the extent and consequences of intratumor heterogeneity
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Roles and mechanisms of alternative splicing in cancer — implications for care
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Self-citationGenetic landscape of esophageal squamous cell carcinoma
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RNA splicing factors as oncoproteins and tumour suppressors
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Epigenomic alterations define lethal CIMP-positive ependymomas of infancy
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Self-citationWhole-exome sequencing identifies a recurrent NAB2-STAT6 fusion in solitary fibrous tumors
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Self-citationThe Histone Mark H3K36me3 Regulates Human DNA Mismatch Repair through Its Interaction with MutSα
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Cancer as a dysregulated epigenome allowing cellular growth advantage at the expense of the host
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The Genomic Landscape of Pediatric Ewing Sarcoma
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Self-citationTobacco smoking and somatic mutations in human bronchial epithelium
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Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms
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- Authors
- Imielinski, M., Berger, A. H., Hammerman, P. S., Hernandez, B., Pugh, T. J., Hodis, E., Cho, J., Suh, J., Capelletti, M., Sivachenko, A., Sougnez, C., Auclair, D., Lawrence, M. S., Stojanov, P., Cibulskis, K., Choi, K., de Waal, L., Sharifnia, T., Brooks, A., Greulich, H., Banerji, S., Zander, T., Seidel, D., Leenders, F., Ansén, S., Ludwig, C., Engel-Riedel, W., Stoelben, E., Wolf, J., Goparju, C., Thompson, K., Winckler, W., Kwiatkowski, D., Johnson, B. E., Jänne, P. A., Miller, V. A., Pao, W., Travis, W. D., Pass, H. I., Gabriel, S. B., Lander, E. S., Thomas, R. K., Garraway, L. A., Getz, G., & Meyerson, M.
- Affiliations
- Broad Institute (US)
- Samsung Medical Center (KR)
- NYU Langone Health (US)
- Dana-Farber Cancer Institute (US)
- University of Cologne (DE)
- Memorial Sloan Kettering Cancer Center (US)
- Vanderbilt University (US)
- Corresponding author
- Meyerson, Matthew
- ORCID
- Imielinski, Marcin
- Berger, Alice H.
- Hammerman, Peter S.
- Hernandez, Bryan
- Pugh, Trevor J.
- Hodis, Eran
- Cho, Jeonghee
- Suh, James
- Capelletti, Marzia
- Sivachenko, Andrey
- Auclair, Daniel
- Lawrence, Michael S.
- Cibulskis, Kristian
- Sharifnia, Tanaz
- Brooks, Angela
- Greulich, Heidi
- Banerji, Shantanu
- Zander, Thomas
- Seidel, Danila
- Stoelben, Erich
- Wolf, Jürgen
- Winckler, Wendy
- Kwiatkowski, David
- Johnson, Bruce E.
- Miller, Vincent A.
- Pao, William
- Travis, William D.
- Pass, Harvey I.
- Gabriel, Stacey B.
- Lander, Eric S.
- Thomas, Roman K.
- Garraway, Levi A.
- Getz, Gad
- Meyerson, Matthew
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2012-09
- Volume
- 150
- Issue
- 6
- Pages
- 1107-1120
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3557932
- OpenAlex
- W2042386784
- Cited by
- 1,789
- References
- 79
- Citations by year
- 2026: 38 · 2025: 66 · 2024: 81 · 2023: 94 · 2022: 124 · 2021: 128 · 2020: 155 · 2019: 131 · 2018: 138 · 2017: 138 · 2016: 145 · 2015: 187 · 2014: 199 · 2013: 148 · 2012: 14
- FWCI
- 141.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 380 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc)
- Max Planck Institute for Plasma Physics (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- Broad Institute
- Canadian Institutes of Health Research
- National Human Genome Research Institute (U54HG003067)
- National Cancer Institute (R01CA109038, R01CA116020, T32 CA9216, P50CA090578, T32CA009216)
- National Institute of General Medical Sciences (T32 GM07753, T32GM007753)
- 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 › Oncology › Lung Cancer Research Studies
- Keywords
- lung adenocarcinoma, somatic mutations, mutational signatures, U2AF1, RBM10, ARID1A, structural rearrangement, EGFR, SIK2, smoking history, cancer genomics, therapeutic target
- MeSH terms
- Adenocarcinoma of Lung, Adenocarcinoma, Adult, Aged, Aged, 80 and over, Carcinoma, Non-Small-Cell Lung, Female, Humans, Lung Neoplasms, Male, Middle Aged, Mutation, Cohort Studies, Genes, Neoplasm, Genome-Wide Association Study, High-Throughput Nucleotide Sequencing, Exome, Mutation Rate
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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