ArticlePloS one2012
Divergent genomic and epigenomic landscapes of lung cancer subtypes underscore the selection of different oncogenic pathways during tumor development.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Overcoming BET-inhibitor JQ1 resistance in aggressive non-small cell lung cancer by inducing ferroptosis via inhibition of the BRD2-FTH1 axis.The FEBS journal · 2025Article
- Integrative genomics identifies SHPRH as a tumor suppressor gene in lung adenocarcinoma that regulates DNA damage response.British journal of cancer · 2024Article
- CYB5R3 functions as a tumor suppressor by inducing ER stress-mediated apoptosis in lung cancer cells via the PERK-ATF4 and IRE1α-JNK pathways.Experimental & molecular medicine · 2024Article
- Article
- Advancing the Care of Pancreatic Cancer Patients: Moving Beyond Just Tumour Tissue.Biomarker insights · 2021Review
- Epithelial tumor suppressor ELF3 is a lineage-specific amplified oncogene in lung adenocarcinoma.Nature communications · 2019Article
- Integrative Genomic Analyses Identifies GGA2 as a Cooperative Driver of EGFR-Mediated Lung Tumorigenesis.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2019Article
- Identification of prognostic gene signature associated with microenvironment of lung adenocarcinoma.PeerJ · 2019Article
- Quantitative or qualitative transcriptional diagnostic signatures? A case study for colorectal cancer.BMC genomics · 2018Article
- Breaking the crosstalk of the cellular tumorigenic network: Hypothesis for addressing resistances to targeted therapies in advanced NSCLC.Oncotarget · 2017Review
- Synthetic lethality in lung cancer and translation to clinical therapies.Molecular cancer · 2016Review
- Assessment of the clinical relevance of 17q25.3 copy number and three-dimensional telomere organization in non-small lung cancer patients.Journal of cancer research and clinical oncology · 2016Article
- Phosphatidylinositol 3-kinase-AKT-mammalian target of rapamycin (PI3K-Akt-mTOR) signaling pathway in non-small cell lung cancer.Translational lung cancer research · 2015Review
- [Genetic characteristics and research progress of targeted therapy in squamous cell carcinoma].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2015Review
- Loss of the Notch effector RBPJ promotes tumorigenesis.The Journal of experimental medicine · 2015Article
- Novel Application of Junction Trees to the Interpretation of Epigenetic Differences among Lung Cancer Subtypes.AMIA Joint Summits on Translational Science proceedings. AMIA Joint Summits on Translational Science · 2015Article
- Epigenetics of lung cancer.Translational research : the journal of laboratory and clinical medicine · 2015Review
- Lung cancer transcriptomes refined with laser capture microdissection.The American journal of pathology · 2014Article
- EYA4 is inactivated biallelically at a high frequency in sporadic lung cancer and is associated with familial lung cancer risk.Oncogene · 2014Article
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
For therapeutic purposes, non-small cell lung cancer (NSCLC) has traditionally been regarded as a single disease. However, recent evidence suggest that the two major subtypes of NSCLC, adenocarcinoma (AC) and squamous cell carcinoma (SqCC) respond differently to both molecular targeted and new generation chemotherapies. Therefore, identifying the molecular differences between these tumor types may impact novel treatment strategy. We performed the first large-scale analysis of 261 primary NSCLC tumors (169 AC and 92 SqCC), integrating genome-wide DNA copy number, methylation and gene expression profiles to identify subtype-specific molecular alterations relevant to new agent design and choice of therapy. Comparison of AC and SqCC genomic and epigenomic landscapes revealed 778 altered genes with corresponding expression changes that are selected during tumor development in a subtype-specific manner. Analysis of >200 additional NSCLCs confirmed that these genes are responsible for driving the differential development and resulting phenotypes of AC and SqCC. Importantly, we identified key oncogenic pathways disrupted in each subtype that likely serve as the basis for their differential tumor biology and clinical outcomes. Downregulation of HNF4α target genes was the most common pathway specific to AC, while SqCC demonstrated disruption of numerous histone modifying enzymes as well as the transcription factor E2F1. In silico screening of candidate therapeutic compounds using subtype-specific pathway components identified HDAC and PI3K inhibitors as potential treatments tailored to lung SqCC. Together, our findings suggest that AC and SqCC develop through distinct pathogenetic pathways that have significant implication in our approach to the clinical management of NSCLC.
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