Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA247969 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:41 lung adenocarcinoma from never-smokers hybridized on Illumina SNP arrays on 13 HumanCNV370-Quadv3 chips. High-resolution array comparative genomic hybridization analysis of lung adenocarcinoma in 41 never smokers for identification of new minimal common regions (MCR) of gain or loss. The SNP array analysis validated copy-number aberrations and revealed that RB1 and WRN were altered by recurrent copy-neutral loss of heterozygosity.The present study has uncovered new aberrations containing cancer genes. The oncogene FUS is a candidate gene in the 16p region that is frequently gained in never smokers. Multiple genetic pathways defined by gains of MYC, deletions of RB1 and WRN or gains on 7p and 7q are involved in lung adenocarcinoma in never smokers. A 'Cartes d'Identite des Tumeurs' (CIT) project from the French National League Against Cancer (http://cit.ligue-cancer.net) 41 samples hybridized on Illumina SNP arrays. Submitter : Fabien PETEL petelf@ligue-cancer.net . Project leader : Pr Pierre FOURET pierre.fouret@psl.aphp.fr
2011-07-28 | E-TABM-1169 | biostudies-arrayexpress
Project description:CGH array in Lung Adenocarcinoma in Never Smokers
2010-12-31 | E-TABM-926 | biostudies-arrayexpress
Project description:We demonstrate that miR-708 is one of the most highly overexpressed miRNAs in non-small cell lung cancer. High level of miR-708 in tumor is also associated with a reduced overall survival in lung adenocarcinomas from never smokers. Functionally, miR-708 overexpression increases the proliferation, migration, and invasion in cultured cells and down regulates TMEM88, a negative regulator of Wnt signaling. Jointly, our results support an oncogenic role of miR-708 by activating Wnt signaling pathway to promote lung cancer progression. We performed miRNA expression profiling in matched lung adenocarcinoma and uninvolved lung using 47 pairs from formalin-fixed, paraffin-embedded [FFPE] tissues from never smokers. We performed miRNA expression profiling in matched lung adenocarcinoma and uninvolved lung using 56 pairs of fresh-frozen [FF] samples from never smokers.
2012-08-02 | E-GEOD-36681 | biostudies-arrayexpress
Project description:Differential profiles from whole genome human expression arrays on monocytes obtained from peripheral blood in COPD was studied and compared with controls. Monocytes were isolated from Controls (Group 1) which included Control Smokers (Group 1A) and Control Never Smokers (Group 1B) and COPD (Group 2) which included COPD Smokers (Group 2A) and COPD ExSmokers (Group 2B). Differential transcriptomic expression associated with (i) Smoking, (ii) COPD, and (iii) cessation of smoking were identified.
2022-01-19 | GSE146560 | GEO
Project description:Genomic study of lung adenocarcinoma in young never-smokers
| PRJEB23826 | ENA
Project description:A genome wide study of lung cancer in never smokers
| PRJNA210011 | ENA
Project description:Conserved recurrent gene mutations correlate with pathway deregulation and clinical outcomes of lung adenocarcinoma in never-smokers
| PRJNA344450 | ENA
Project description:Alteration of gene expression profile of target organs may signal exposure of that organ to toxic chemicals. We analyzed the transcriptome of the non-involved lung tissue, excised from 176 surgically treated lung adenocarcinoma patients, to identify genes whose expression levels were altered by individual habit to cigarette smoking. Of 17.097 genes analyzed, 357 resulted to be differentially expressed between never smokers and ever smokers (FDR <0.05). The gene that resulted to be the most significantly differentially expressed was MYO1A (FDR = 6.9 x 10-4 and ever versus never smokers fold change of 1.42). We compared our results with those of five independent datasets and found that more than one third (38.6%) of the transcripts associated with smoking habit in our dataset overlapped with at least one of the other datasets, with 7 genes (KMO, CD1A, SPINK5, TREM2, CYBB, DNASE2B, FGG) resulting significantly differentially expressed between ever and never smokers in all five datasets, with concordant higher expression in ever smokers than in never smokers. Most of the genes that we found significantly differentially expressed between ever and never smokers participate in pathways/networks that are directly or indirectly associated with immunity and inflammation, in particular, the most significantly enriched pathway was that of eicosanoid signaling. Overall, present results further points to the inflammatory condition that characterize the lung tissue of smokers.
2019-10-01 | GSE123352 | GEO
Project description:Approximately 15% of lung cancer cases are not associated with smoking and show molecular and clinical characteristics distinct from those in smokers. Epidermal growth factor receptor (EGFR) gene mutations, which are correlated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), are more frequent in never-smoker lung cancers. In this study, microRNA (miRNA) expression profiling of 28 never-smoker lung cancer cases identified aberrantly expressed miRNAs, which were much fewer than in lung cancers of smokers and included miRNAs previously identified (e.g., upregulated miR-21) and unidentified (e.g., downregulated miR-138) in those smoker cases. The changes in expression of some of these miRNAs were more remarkable in cases with EGFR mutations than in those without: the most upregulated miRNA, miR-21, was more abundant in cancers with EGFR mutation. A significant correlation between phosphorylated-EGFR (p-EGFR) and miR-21 levels in lung carcinoma cell lines and the suppression of miR-21 by an EGFR-TKI, AG1478, suggested that the EGFR signaling pathway positively regulated miR-21 expression. In a never-smoker-derived lung adenocarcinoma cell line H3255 with mutant EGFR and high levels of p-EGFR and miR-21, antisense inhibition of miR-21 enhanced AG1478-induced apoptosis. In a never-smoker-derived adenocarcinoma cell line H441 with wild-type EGFR, the antisense miR-21 not only showed the additive effect with AG1478 but also induced apoptosis by itself. These results suggest that aberrantly increased expression of miR-21, which is further enhanced by the activated EGFR signaling pathway, plays a critical role in lung carcinogenesis in never-smokers and is a potential therapeutic target in both EGFR mutant and wild-type cases. Twenty-eight pairs of lung cancer tissues and corresponding noncancerous lung tissues were obtained from never-smokers who had undergone surgical resection from 2000 to 2004 at the University of Maryland Medical Center (n=15), Mayo Clinic (n=7) in United States and Hamamatsu University School of Medicine (n=6) in Japan.
2010-05-15 | E-GEOD-14936 | biostudies-arrayexpress
Project description:Approximately 15% of lung cancer cases are not associated with smoking and show molecular and clinical characteristics distinct from those in smokers. Epidermal growth factor receptor (EGFR) gene mutations, which are correlated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), are more frequent in never-smoker lung cancers. In this study, microRNA (miRNA) expression profiling of 28 never-smoker lung cancer cases identified aberrantly expressed miRNAs, which were much fewer than in lung cancers of smokers and included miRNAs previously identified (e.g., upregulated miR-21) and unidentified (e.g., downregulated miR-138) in those smoker cases. The changes in expression of some of these miRNAs were more remarkable in cases with EGFR mutations than in those without: the most upregulated miRNA, miR-21, was more abundant in cancers with EGFR mutation. A significant correlation between phosphorylated-EGFR (p-EGFR) and miR-21 levels in lung carcinoma cell lines and the suppression of miR-21 by an EGFR-TKI, AG1478, suggested that the EGFR signaling pathway positively regulated miR-21 expression. In a never-smoker-derived lung adenocarcinoma cell line H3255 with mutant EGFR and high levels of p-EGFR and miR-21, antisense inhibition of miR-21 enhanced AG1478-induced apoptosis. In a never-smoker-derived adenocarcinoma cell line H441 with wild-type EGFR, the antisense miR-21 not only showed the additive effect with AG1478 but also induced apoptosis by itself. These results suggest that aberrantly increased expression of miR-21, which is further enhanced by the activated EGFR signaling pathway, plays a critical role in lung carcinogenesis in never-smokers and is a potential therapeutic target in both EGFR mutant and wild-type cases.
2009-07-29 | GSE14936 | GEO