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1. Full Text Detection of known and novel ALK fusion transcripts in lung cancer patients using next-generation sequencing approaches
by Vendrell, Julie A and Taviaux, Sylvie and Béganton, Benoît and Godreuil, Sylvain and Audran, Patricia and Grand, David and Clermont, Estelle and Serre, Isabelle and Szablewski, Vanessa and Coopman, Peter and Mazières, Julien and Costes, Valérie and Pujol, Jean-Louis and Brousset, Pierre and Rouquette, Isabelle and Solassol, Jérôme
Scientific Reports, ISSN 2045-2322, 12/2017, Volume 7, Issue 1, pp. 12510 - 11
Rearrangements of the anaplastic lymphoma kinase (ALK) gene in non-small cell lung cancer (NSCLC) represent a novel molecular target in a small subset of... 
GENE FUSIONS | SPITZ TUMORS | ASSAY | ANAPLASTIC LYMPHOMA-KINASE | MULTIDISCIPLINARY SCIENCES | FISH | CRIZOTINIB | RET FUSIONS | INFLAMMATORY MYOFIBROBLASTIC TUMORS | REARRANGEMENTS | MULTIPLEX | Lung Neoplasms - drug therapy | Oncogene Proteins, Fusion - metabolism | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Humans | Lung Neoplasms - metabolism | Middle Aged | Male | Antineoplastic Agents - therapeutic use | RNA, Messenger - metabolism | Case-Control Studies | Anaplastic Lymphoma Kinase - genetics | Adenocarcinoma of Lung - genetics | Adenocarcinoma of Lung - drug therapy | Anaplastic Lymphoma Kinase - metabolism | Female | High-Throughput Nucleotide Sequencing - instrumentation | High-Throughput Nucleotide Sequencing - methods | Dynactin Complex - genetics | Lung Neoplasms - genetics | Gene Expression | Carcinoma, Non-Small-Cell Lung - surgery | Crizotinib - therapeutic use | Carcinoma, Non-Small-Cell Lung - genetics | RNA, Messenger - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | In Situ Hybridization, Fluorescence | Adenocarcinoma of Lung - surgery | Dynactin Complex - metabolism | Golgi Matrix Proteins - genetics | Oncogene Proteins, Fusion - genetics | Lung Neoplasms - surgery | Aged | Carcinoma, Non-Small-Cell Lung - drug therapy | Adenocarcinoma of Lung - metabolism | Neoplasm Staging | Golgi Matrix Proteins - metabolism | Immunohistochemistry | Transcription | Lung cancer | Fluorescence in situ hybridization | Non-small cell lung carcinoma | Kinases | Lymphoma | Protein-tyrosine kinase | Tumors | Life Sciences
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2. Full Text Synergy between the KEAP1/NRF2 and PI3K Pathways Drives Non-Small-Cell Lung Cancer with an Altered Immune Microenvironment
by Best, Sarah A and De Souza, David P and Kersbergen, Ariena and Policheni, Antonia N and Dayalan, Saravanan and Tull, Dedreia and Rathi, Vivek and Gray, Daniel H and Ritchie, Matthew E and McConville, Malcolm J and Sutherland, Kate D
Cell Metabolism, ISSN 1550-4131, 04/2018, Volume 27, Issue 4, pp. 935 - 943.e4
The lung presents a highly oxidative environment, which is tolerated through engagement of tightly controlled stress response pathways. A critical stress... 
Keap1 | PD-L1 | Pten | Nrf2 | Taldo1 | non-small-cell lung cancer | STEM-CELLS | ORIGIN | NRF2 | LANDSCAPE | ADENOCARCINOMA | INFLAMMATION | ENDOCRINOLOGY & METABOLISM | BLOCKADE | CARCINOMA | EXPRESSION | DELETION | CELL BIOLOGY | NF-E2-Related Factor 2 - physiology | PTEN Phosphohydrolase - genetics | Loss of Function Mutation | Humans | Lung Neoplasms - metabolism | PTEN Phosphohydrolase - physiology | Carcinoma, Non-Small-Cell Lung - metabolism | Gene Expression Regulation, Neoplastic | Kelch-Like ECH-Associated Protein 1 - physiology | PTEN Phosphohydrolase - metabolism | Kelch-Like ECH-Associated Protein 1 - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Carcinogenesis | Carcinoma, Non-Small-Cell Lung - immunology | Kelch-Like ECH-Associated Protein 1 - genetics | Lung Neoplasms - immunology | Animals | Mice, Mutant Strains | NF-E2-Related Factor 2 - metabolism | NF-E2-Related Factor 2 - genetics | Adenocarcinoma of Lung - immunology | Adenocarcinoma of Lung - metabolism | Pentose Phosphate Pathway | Phosphates | Respiratory agents | Metabolites | Lung cancer, Non-small cell | Stem cells
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3. Full Text IFN‐γ‐mediated inhibition of lung cancer correlates with PD‐L1 expression and is regulated by PI3K‐AKT signaling
by Gao, Yi and Yang, Jianjian and Cai, Yixin and Fu, Shengling and Zhang, Ni and Fu, Xiangning and Li, Lequn
International Journal of Cancer, ISSN 0020-7136, 08/2018, Volume 143, Issue 4, pp. 931 - 943
IFN‐γ plays a crucial role in anti‐tumor responses and also induces expression of PD‐L1, a well‐established inhibitor of anti‐tumor immune function.... 
IFNG | PI3K | STAT1 | lung adenocarcinoma | PD‐L1 | PD-L1 | TARGET | CELLS | ACTIVATION | PHOSPHORYLATION | TUMOR-DEVELOPMENT | EGFR | THERAPY | INTERFERON-GAMMA | ONCOLOGY | PATHWAY | RESISTANCE | Phosphorylation | Prognosis | Adenocarcinoma of Lung - pathology | Humans | Lung Neoplasms - metabolism | Transcriptome | Tumor Microenvironment | Lung Neoplasms - pathology | Gene Expression Profiling | Phosphatidylinositol 3-Kinases - metabolism | STAT1 Transcription Factor - metabolism | Adenocarcinoma of Lung - genetics | Janus Kinase 2 - metabolism | Transcription, Genetic | Adenocarcinoma of Lung - immunology | Proto-Oncogene Proteins c-akt - metabolism | STAT3 Transcription Factor - metabolism | Lung Neoplasms - genetics | T-Lymphocytes, Cytotoxic - immunology | Signal Transduction | Interferon-gamma - physiology | B7-H1 Antigen - metabolism | Lung Neoplasms - immunology | Cell Line, Tumor | Adenocarcinoma of Lung - metabolism | Adenocarcinoma | Lung cancer | Crosstalk | Cytotoxicity | AKT protein | Lymphocytes T | Signal transduction | Pathways | Lymphocytes | Immunotherapy | Janus kinase 2 | Cell cycle | Bioindicators | Inhibition | Stat1 protein | Sensitivity analysis | Immune response | Tumor cells | Gene expression | Patients | Molecular chains | 1-Phosphatidylinositol 3-kinase | Signaling | Biomarkers | Interferon | Combinatorial analysis | Cancer | Tumors
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4. Full Text Syndecan-1 Controls Lung Tumorigenesis by Regulating miRNAs Packaged in Exosomes
by Parimon, Tanyalak and Brauer, Rena and Schlesinger, Saundra Y and Xie, Ting and Jiang, Dianhua and Ge, Lingyin and Huang, Ying and Birkland, Timothy P and Parks, William C and Habiel, David M and Hogaboam, Cory M and Gharib, Sina A and Deng, Nan and Liu, Zhenqui and Chen, Peter
The American Journal of Pathology, ISSN 0002-9440, 04/2018, Volume 188, Issue 4, pp. 1094 - 1103
Syndecan-1 is a transmembrane proteoglycan expressed prominently by lung epithelium and has pleiotropic functions such as regulating cell migration,... 
MIGRATION | ADHESION | BIOGENESIS | INTEGRINS | RNA COMPOSITION | RECEPTOR | GROWTH-FACTOR | MICRORNAS | PATHOLOGY | CANCER | EXPRESSION | A549 Cells | Cell Proliferation | Syndecan-1 - metabolism | Adenocarcinoma of Lung - pathology | Humans | Lung Neoplasms - metabolism | Gene Expression Regulation, Neoplastic | Kaplan-Meier Estimate | Exosomes - genetics | Lung Neoplasms - pathology | MicroRNAs - metabolism | Up-Regulation - genetics | Carcinogenesis - metabolism | Down-Regulation - genetics | Animals | Survival Analysis | Mice | MicroRNAs - genetics | Adenocarcinoma of Lung - metabolism
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5. Full Text High expression of synthesis of cytochrome c oxidase 2 and TP53-induced glycolysis and apoptosis regulator can predict poor prognosis in human lung adenocarcinoma
by Liu, Jiabin and Lu, Funian and Gong, Yan and Zhao, Xianda and Zhao, Chen and Pan, Qi and Ballantyne, Stephanie and Tian, Sufang and Chen, Honglei
Human Pathology, ISSN 0046-8177, 07/2018, Volume 77, pp. 54 - 62
Synthesis of cytochrome oxidase 2 (SCO2) and -induced glycolysis and apoptosis regulator (TIGAR) are 2 p53-mediated proteins that can play a regulatory role in... 
Energy metabolism | TIGAR | Lung adenocarcinoma | SCO2 | p53 | CELLS | METABOLISM | ROS | CLASSIFICATION | PATHOLOGY | CANCER | Humans | Lung Neoplasms - metabolism | Middle Aged | Tumor Suppressor Protein p53 - metabolism | Male | Electron Transport Complex IV - metabolism | Carrier Proteins - metabolism | Mitochondrial Proteins - metabolism | Aged, 80 and over | Cell Line, Tumor | Glycolysis | Adult | Female | Aged | Apoptosis - physiology | Adenocarcinoma of Lung - metabolism | Energy Metabolism - physiology | Adenocarcinoma | Cytochrome c | Glucose metabolism | Prognosis | Analysis | Mortality | Physiological aspects | Cytochrome oxidase | Tumor proteins | Apoptosis | Cytochrome | Enzymes | Lymphatic system | Phosphorylation | Quantum dots | Lung cancer | Breast cancer | Metastasis | Multivariate analysis | Metabolism | Patients | Proteins | Hypotheses | Medical prognosis | Surgery | Cell cycle | Age
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6. Full Text p53‐inducible gene 3 promotes cell migration and invasion by activating the FAK/Src pathway in lung adenocarcinoma
by Gu, Meng‐Meng and Gao, Dexuan and Yao, Ping‐An and Yu, Lan and Yang, Xiao‐Dong and Xing, Chun‐Gen and Zhou, Jundong and Shang, Zeng‐Fu and Li, Ming
Cancer Science, ISSN 1347-9032, 12/2018, Volume 109, Issue 12, pp. 3783 - 3793
The p53‐inducible gene 3 ( PIG 3) is one of the p53‐induced genes at the onset of apoptosis, which plays an important role in cell apoptosis and DNA damage... 
migration | p53‐inducible gene 3 | invasion | focal adhesion kinase | non‐small cell lung cancer | non-small cell lung cancer | p53-inducible gene 3 | PIG3 | APOPTOSIS | FAK | ONCOLOGY | PROHIBITIN | CANCER STATISTICS | INHIBITOR | PHASE-I | EXPRESSION | BINDING | Neoplasm Transplantation | Up-Regulation | Phosphorylation | Carcinoma, Squamous Cell - genetics | Carcinoma, Squamous Cell - metabolism | Humans | Lung Neoplasms - metabolism | Middle Aged | Gene Expression Regulation, Neoplastic | Male | Intracellular Signaling Peptides and Proteins - metabolism | Adenocarcinoma of Lung - genetics | Adult | Female | Focal Adhesion Kinase 1 - metabolism | Intracellular Signaling Peptides and Proteins - genetics | Lung Neoplasms - genetics | Proto-Oncogene Proteins - metabolism | A549 Cells | Signal Transduction | Neoplasm Invasiveness | Proto-Oncogene Proteins - genetics | Lymphatic Metastasis | Animals | Proto-Oncogene Proteins pp60(c-src) - metabolism | Cell Line, Tumor | Aged | Mice | Adenocarcinoma of Lung - metabolism | Cell Movement | Adenocarcinoma | Squamous cell carcinoma | RNA | Genes | Genomics | Development and progression | Metastasis | Lung cancer, Non-small cell | Education parks | School facilities | Analysis | Genetic aspects | Tumor proteins | Cancer | p53 Protein | DNA damage | Lung cancer | Clinical trials | Genomes | Kinases | Cancer therapies | Lymph nodes | Metastases | Cell adhesion & migration | Growth factors | Deoxyribonucleic acid--DNA | Lymphatic system | Small cell lung carcinoma | Therapeutic applications | Non-small cell lung carcinoma | Lung carcinoma | Gene expression | Biomarkers | Mutation | Focal adhesion kinase | Paxillin | Binding sites | Cell migration | Apoptosis | Tumors | Original
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7. Full Text Aberrant S100A16 expression might be an independent prognostic indicator of unfavorable survival in non-small cell lung adenocarcinoma
by Chen, De and Luo, Linjie and Liang, Chao
PLoS ONE, ISSN 1932-6203, 05/2018, Volume 13, Issue 5, p. e0197402
S100A16 is a conserved member of the S100 protein family in mammals. Its upregulation was observed in many tumors and is related to malignant transformation.... 
EPITHELIAL-MESENCHYMAL TRANSITION | BREAST-CANCER | METHYLATION | INVASION | PROTEIN | AMPLIFICATION | CANCER GENOME ATLAS | BIOMARKER | PATHWAY | MULTIDISCIPLINARY SCIENCES | CHEMORESISTANCE | Immunohistochemistry | Multivariate Analysis | S100 Calcium Binding Protein A6 - metabolism | Prognosis | Lung Neoplasms - mortality | Humans | Lung Neoplasms - metabolism | Middle Aged | Gene Expression Regulation, Neoplastic | Male | Gene Expression Profiling | Adenocarcinoma of Lung - mortality | DNA Methylation | Biomarkers, Tumor - metabolism | Female | Retrospective Studies | Carcinoma, Non-Small-Cell Lung - metabolism | Cell Cycle Proteins - metabolism | Kaplan-Meier Estimate | Gene Dosage | Carcinoma, Non-Small-Cell Lung - mortality | Disease-Free Survival | Cell Line, Tumor | CpG Islands | Aged | Adenocarcinoma of Lung - metabolism | Adenocarcinoma | Genetic aspects | Lung cancer, Non-small cell | Methylation | Health aspects | EF hand proteins | Transformation | Copy number | Lung cancer | Genomes | Tissue analysis | Multivariate analysis | Data mining | Tissues | Cancer therapies | Gene sequencing | Proteins | S100 protein | Cell growth | DNA methylation | Indicators | Deoxyribonucleic acid--DNA | CpG islands | Cell survival | Regression analysis | Gene expression | Survival | Survival analysis | Lungs | Correlation analysis | Medical prognosis | Epigenetics | Cancer | Tumors | Deoxyribonucleic acid | DNA
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8. Full Text BRM270 inhibits cancer stem cell maintenance via microRNA regulation in chemoresistant A549 lung adenocarcinoma cells
by Kwon, T and Chandimali, N and Huynh, DL and Zhang, JJ and Kim, N and Bak, Y and Yoon, DY and Yu, DY and Lee, JC and Gera, M and Ghosh, M and Park, YH and Jeong, DK
CELL DEATH & DISEASE, ISSN 2041-4889, 02/2018, Volume 9, Issue 2, pp. 244 - 9
Chemotherapy is a standard treatment for non-small-cell lung cancer (NSCLC). However, the dose-limiting toxicity of drugs and the development of... 
GEFITINIB | PROFILES | BMI-1 | STATISTICS | RESISTANCE | SELF-RENEWAL | TUMORIGENESIS | TUMOR-INITIATING CELLS | CELL BIOLOGY | Lung Neoplasms - drug therapy | Adenocarcinoma of Lung - pathology | Neoplastic Stem Cells - drug effects | Humans | Lung Neoplasms - metabolism | Gene Expression Regulation, Neoplastic | Spheroids, Cellular - pathology | Drugs, Chinese Herbal - pharmacology | Lung Neoplasms - pathology | MicroRNAs - metabolism | NF-kappa B - metabolism | Apoptotic Protease-Activating Factor 1 - genetics | Carcinogenesis - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Adenocarcinoma of Lung - genetics | Neoplastic Stem Cells - metabolism | Adenocarcinoma of Lung - drug therapy | Neoplastic Stem Cells - pathology | Female | MicroRNAs - agonists | Spheroids, Cellular - drug effects | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | A549 Cells | Signal Transduction | Carcinoma, Non-Small-Cell Lung - genetics | Spheroids, Cellular - metabolism | Carcinogenesis - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Apoptotic Protease-Activating Factor 1 - metabolism | Carcinogenesis - drug effects | Carcinogenesis - pathology | Xenograft Model Antitumor Assays | Drug Resistance, Neoplasm - genetics | Animals | NF-kappa B - genetics | Tumor Burden - drug effects | Mice, Nude | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | MicroRNAs - genetics | Carcinoma, Non-Small-Cell Lung - drug therapy | Adenocarcinoma of Lung - metabolism | Antineoplastic Agents, Phytogenic - pharmacology | Proto-Oncogene Proteins c-bcl-2 - genetics | Drug Resistance, Neoplasm - drug effects | Medicinal plants | Cell proliferation | Adenocarcinoma | Toxicity | MiRNA | Chemoresistance | Non-small cell lung carcinoma | Drug resistance | Drug development | Cancer therapies | Chemotherapy | Lungs | Stem cells | Tumorigenesis | Cell migration
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9. Full Text The epithelial-to-mesenchymal transition activator ZEB1 initiates a prometastatic competing endogenous RNA network
by Tan, Xiaochao and Banerjee, Priyam and Liu, Xin and Yu, Jiang and Gibbons, Don L and Wu, Ping and Scott, Kenneth L and Diao, Lixia and Zheng, Xiaofeng and Wang, Jing and Jalali, Ali and Suraokar, Milind and Fujimoto, Junya and Behrens, Carmen and Liu, Xiuping and Liu, Chang-Gong and Creighton, Chad J and Wistuba, Ignacio I and Kurie, Jonathan M
Journal of Clinical Investigation, ISSN 0021-9738, 04/2018, Volume 128, Issue 4, pp. 1268 - 1282
Epithelial tumor cells undergo epithelial-to-mesenchymal transition (EMT) to gain metastatic activity. Competing endogenous RNAs (ceRNAs) have binding sites... 
PROTEIN-KINASE-A | MEDICINE, RESEARCH & EXPERIMENTAL | MESSENGER-RNAS | CELLS | METASTASIS | LONG NONCODING RNA | PANCREATIC-CANCER | MIR-200 FAMILY | EXPRESSION | EMT | PROMOTES | Lung Neoplasms - genetics | Adenocarcinoma of Lung - pathology | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Neoplasm Proteins - metabolism | Zinc Finger E-box-Binding Homeobox 1 - genetics | RNA, Neoplasm - metabolism | Zinc Finger E-box-Binding Homeobox 1 - metabolism | Neoplasm Metastasis | Adenocarcinoma of Lung - genetics | Animals | Epithelial-Mesenchymal Transition | Cell Line, Tumor | RNA, Neoplasm - genetics | Mice | Adenocarcinoma of Lung - metabolism | Neoplasm Proteins - genetics | Cell Movement | Transcription factors | MicroRNA | Prognosis | Lung cancer | Physiological aspects | Development and progression | Genetic aspects | Metastasis | Health aspects | Adenocarcinoma | Competition | Mesenchyme | Tumor cells | MiRNA | Tumor cell lines | Kinases | Metastases | Proteins | Adenylate cyclase | Liver cancer | 3' Untranslated regions | MicroRNAs | Cell migration
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10. Full Text Loss of RUNX1 is associated with aggressive lung adenocarcinomas
by Ramsey, Jon and Butnor, Kelly and Peng, Zhihua and Leclair, Tim and van der Velden, Jos and Stein, Gary and Lian, Jane and Kinsey, C. Matthew
Journal of Cellular Physiology, ISSN 0021-9541, 04/2018, Volume 233, Issue 4, pp. 3487 - 3497
Runt‐related transcription factors are important in a number of oncogenic processes. Here, we describe the first results to implicate RUNX1 in lung cancer and... 
adenocarcinoma | runt related transcription factor | RUNX | non‐small cell lung cancer | non-small cell lung cancer | CANCER-CELLS | PHYSIOLOGY | GENE | ROLES | E2F1 | TRANSCRIPTIONAL REGULATION | EXPRESSION | CELL BIOLOGY | Aggression - physiology | Adenocarcinoma - metabolism | Core Binding Factor Alpha 2 Subunit - metabolism | Humans | Lung Neoplasms - metabolism | Cell Proliferation - physiology | Gene Expression Regulation - physiology | Gene Expression Profiling - methods | Hematopoietic Stem Cells - metabolism | Transcriptional Activation - physiology | Adenocarcinoma of Lung - metabolism | RNA | Leukemia | Analysis | Lung cancer | Genes | Genomics | Development and progression | Gene expression | Hematopoietic stem cells | Adenocarcinoma | Translocation | Deregulation | Transcription factors | Runx1 protein | Genomes | Survival | Confidence intervals | Medical centres | Etiology | Network analysis | Surgery | Stem cells | Tumor suppressor genes | Tumors | Cancer | Runt related transcription factor | Non-small cell lung cancer
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11. Full Text CLDN18.1 attenuates malignancy and related signaling pathways of lung adenocarcinoma in vivo and in vitro
by Luo, Jiao and Chimge, Nyam‐Osor and Zhou, Beiyun and Flodby, Per and Castaldi, Alessandra and Firth, Amy L and Liu, Yixin and Wang, Hongjun and Yang, Chenchen and Marconett, Crystal N and Crandall, Edward D and Offringa, Ite A and Frenkel, Baruch and Borok, Zea
International Journal of Cancer, ISSN 0020-7136, 12/2018, Volume 143, Issue 12, pp. 3169 - 3180
Claudins are a family of transmembrane proteins integral to the structure and function of tight junctions (TJ). Disruption of TJ and alterations in claudin... 
AKT | xenograft | IGF‐1 receptor | YAP/TAZ | lung alveolar epithelial type II cells | IGF-1 receptor | TARGET | PHOSPHORYLATION | JUNCTION PROTEIN CLAUDIN-7 | HIPPO PATHWAY | YAP | TAZ | ONCOLOGY | GROWTH | INHIBITS CELL-PROLIFERATION | EXPRESSION | Lung Neoplasms - genetics | Claudins - genetics | Claudins - physiology | Promoter Regions, Genetic | Receptor, IGF Type 1 - metabolism | Phosphorylation | Cell Proliferation | Proto-Oncogene Proteins c-yes - metabolism | Adenocarcinoma of Lung - pathology | Neoplasm Invasiveness | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Intracellular Signaling Peptides and Proteins - metabolism | Blotting, Western | Mice, Knockout | DNA Methylation | Neoplasm Metastasis | Adenocarcinoma of Lung - genetics | Animals | Signal Transduction - physiology | Mice | Adenocarcinoma of Lung - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Adenocarcinoma | Genetic research | Metastasis | Methylation | Analysis | Membrane proteins | Cell proliferation | Transcription | Xenotransplantation | AKT protein | Insulin-like growth factors | Malignancy | Kinases | Inactivation | Metastases | Proteins | Xenografts | DNA methylation | Alveoli | Growth factors | Deactivation | Tight junctions | Invasiveness | siRNA | Insulin | Yes-associated protein | Signaling | Lungs | Tumor suppressor genes | Disruption | Cell migration | Cancer | Tumors | Structure-function relationships
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