Analysis of Complex Genomic Rearrangements of Lung Adenocarcinomas
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ABSTRACT:
PROVIDER: EGAS00001002801 | EGA |
REPOSITORIES: EGA
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Project description:Lung cancer is the worldwide leading cause of death from cancer. Tobacco usage is the major pathogenic factor, however, not all lung cancers can be attributable to smoking. The genetic aberrations that differ between smokers' and never-smokers’ lung carcinomas remain to a large extent unclear. We analyzed 72 early-stage primary lung carcinomas including small cell lung cancers LCNEC, adenocarcinomas and squamous cell carcinomas by Illumina HT12 gene expression microarrays.
2012-05-17 | GSE29016 | GEO
Project description:Cigarette smoke is associated with the majority of lung cancers: however, 25% of lung cancer patients are non-smokers, and half of all newly diagnosed lung cancer patients are former smokers. Lung tumors exhibit distinct epidemiological, clinical, pathological, and molecular features depending on smoking status, suggesting divergent mechanisms underlie tumorigenesis in smokers and non-smokers. MicroRNAs (miRNAs) are integral contributors to tumorigenesis and mediate biological responses to smoking. Based on the hypothesis that smoking-specific miRNA differences in lung adenocarcinomas reflect distinct tumorigenic processes selected by different smoking and non-smoking environments, we investigated the contribution of miRNA disruption to lung tumor biology and patient outcome in the context of smoking status. Results: We discovered novel and distinct smoking-status-specific patterns of miRNA and miRNA-mediated gene networks, and identified miRNAs that were prognostically significant in a smoking-dependent manner. Conclusions: We conclude that miRNAs disrupted in a smoking-status-dependent manner affect distinct cellular pathways and differentially influence lung cancer patient prognosis in current, former and never smokers. Our findings may represent promising biologically relevant markers for lung cancer prognosis or therapeutic intervention.
2014-10-30 | GSE62182 | GEO
Project description:Cigarette smoke is associated with the majority of lung cancers: however, 25% of lung cancer patients are non-smokers, and half of all newly diagnosed lung cancer patients are former smokers. Lung tumors exhibit distinct epidemiological, clinical, pathological, and molecular features depending on smoking status, suggesting divergent mechanisms underlie tumorigenesis in smokers and non-smokers. MicroRNAs (miRNAs) are integral contributors to tumorigenesis and mediate biological responses to smoking. Based on the hypothesis that smoking-specific miRNA differences in lung adenocarcinomas reflect distinct tumorigenic processes selected by different smoking and non-smoking environments, we investigated the contribution of miRNA disruption to lung tumor biology and patient outcome in the context of smoking status. Results: We discovered novel and distinct smoking-status-specific patterns of miRNA and miRNA-mediated gene networks, and identified miRNAs that were prognostically significant in a smoking-dependent manner. Conclusions: We conclude that miRNAs disrupted in a smoking-status-dependent manner affect distinct cellular pathways and differentially influence lung cancer patient prognosis in current, former and never smokers. Our findings may represent promising biologically relevant markers for lung cancer prognosis or therapeutic intervention. We applied a whole transcriptome sequencing based approach to interrogate miRNA levels in 94 patient-matched lung adenocarcinoma and non-malignant lung parenchymal tissue pairs from current [CS], former [FS] and never smokers [NS].
2014-10-30 | E-GEOD-62182 | biostudies-arrayexpress
Project description:Purpose: DNA methylation alterations are early events in tumorigenesis and important in the regulation of gene expression in cancer cells. Lung cancer has in general a poor prognosis, and a deeper insight into the epigenetic landscape in lung adenocarcinoma tumors and its prognostic implications is needed. Experimental Design: We determined whole-genome DNA methylation profiles of 164 lung adenocarcinoma samples and 19 samples of matched normal lung tissue samples using the Illumina Infinium 450K array. The methylation levels were correlated with gene expression levels analyzed by the Agilent 60K mRNA expression array. Methylation changes were studied specifically in tumors from never-smoking patients, and in tumors with mutations in the EGFR-, KRAS- or TP53 genes, and survival analyses were performed. Results: We identified a large number of differentially methylated CpGs in lung adenocarcinoma tissue, and different methylation profiles in tumors from smokers and never-smokers. Specific methylation profiles were observed in tumors with mutations in the EGFR-, KRAS- or TP53 gene. Both positive and negeative correlations between DNA methylation levels and mRNA expression levels were seen. Methylation profiles of the tumor samples identified clusters of patients with distinct prognosis. A prognostic index based on the methylation levels of 33 CpGs was established, and validated in an independent cohort of lung adenocarcinoma patients from the TCGA project. Among the CpGs in the prognostic signature, some were localized in the HOX B and HOX C gene clusters. Conclusions: Methylation differences mirror biological important features the etiology of lung adenocarcinomas and influence prognosis.
2015-11-27 | GSE66836 | GEO
Project description:Transcriptomes of lung adenocarcinomas
| PRJNA638137 | ENA
Project description:Transcriptomes of lung adenocarcinomas
| PRJNA593979 | ENA
Project description:Purpose: DNA methylation alterations are early events in tumorigenesis and important in the regulation of gene expression in cancer cells. Lung cancer has in general a poor prognosis, and a deeper insight into the epigenetic landscape in lung adenocarcinoma tumors and its prognostic implications is needed. Experimental Design: We determined whole-genome DNA methylation profiles of 164 lung adenocarcinoma samples and 19 samples of matched normal lung tissue samples using the Illumina Infinium 450K array [GSE66836]. The methylation levels were correlated with gene expression levels analyzed by the Agilent 60K mRNA expression array. Methylation changes were studied specifically in tumors from never-smoking patients, and in tumors with mutations in the EGFR-, KRAS- or TP53 genes, and survival analyses were performed. Results: We identified a large number of differentially methylated CpGs in lung adenocarcinoma tissue, and different methylation profiles in tumors from smokers and never-smokers. Specific methylation profiles were observed in tumors with mutations in the EGFR-, KRAS- or TP53 gene. Both positive and negeative correlations between DNA methylation levels and mRNA expression levels were seen. Methylation profiles of the tumor samples identified clusters of patients with distinct prognosis. A prognostic index based on the methylation levels of 33 CpGs was established, and validated in an independent cohort of lung adenocarcinoma patients from the TCGA project. Among the CpGs in the prognostic signature, some were localized in the HOX B and HOX C gene clusters. Conclusions: Methylation differences mirror biological important features the etiology of lung adenocarcinomas and influence prognosis.
2015-11-13 | GSE66863 | GEO
Project description:We performed RNA-seq using 19 human surgically-resected lung adenocarcinomas to investigate of difference between EGFR-mutated and wild-type lung adenocarcinomas.
2020-02-25 | GSE141569 | GEO
Project description:Lung cancer occurs in never-smokers. Epigenetic changes in lung cancer potentially represent important diagnostic, prognostic, and therapeutic targets. We compared DNA methylation profiles of 28 adenocarcinomas of the lungs of never-smokers with paired adjacent nonmalignant lung tissue. We correlated differential methylation changes with gene expression changes from the same 28 samples. We observed a distinct separation in methylation profiles between tumor and adjacent nonmalignant lung tissue using principal component analysis. Tumors were generally hypomethylated compared with adjacent nonmalignant tissue. Of 1,906 differentially methylated CpG sites between tumor and nonmalignant tissue, 1,198 were within classically defined CpG islands where tumors were hypermethylated compared with nonmalignant tissue. A total of 708 sites were outside CpG islands where tumors were hypomethylated compared with nonmalignant tissue. There were significant differences in expression of 351 genes (23%) of the 1,522 genes matched to the differentially methylated CpG sites. Genes that were not significantly differentially expressed and were hypermethylated within CpG sites were enriched for homeobox genes. These results suggest that the methylation profiles of lung adenocarcinomas of never-smokers and adjacent nonmalignant lung tissue are significantly different. Despite the differential methylation of homeobox genes, no significant changes in expression of these genes were detected. Twenty eight pairs of tumor and adjacent normal lungs were profiled for lung adenocarcinoma patients by gene expression and DNA methylation microarray
2015-02-03 | E-GEOD-62948 | biostudies-arrayexpress
Project description:Lung cancer occurs in never-smokers. Epigenetic changes in lung cancer potentially represent important diagnostic, prognostic, and therapeutic targets. We compared DNA methylation profiles of 28 adenocarcinomas of the lungs of never-smokers with paired adjacent nonmalignant lung tissue. We correlated differential methylation changes with gene expression changes from the same 28 samples. We observed a distinct separation in methylation profiles between tumor and adjacent nonmalignant lung tissue using principal component analysis. Tumors were generally hypomethylated compared with adjacent nonmalignant tissue. Of 1,906 differentially methylated CpG sites between tumor and nonmalignant tissue, 1,198 were within classically defined CpG islands where tumors were hypermethylated compared with nonmalignant tissue. A total of 708 sites were outside CpG islands where tumors were hypomethylated compared with nonmalignant tissue. There were significant differences in expression of 351 genes (23%) of the 1,522 genes matched to the differentially methylated CpG sites. Genes that were not significantly differentially expressed and were hypermethylated within CpG sites were enriched for homeobox genes. These results suggest that the methylation profiles of lung adenocarcinomas of never-smokers and adjacent nonmalignant lung tissue are significantly different. Despite the differential methylation of homeobox genes, no significant changes in expression of these genes were detected. Twenty eight pairs of tumor and adjacent normal lungs were profiled for lung adenocarcinoma patients by gene expression and DNA methylation microarray
2015-02-03 | E-GEOD-62949 | biostudies-arrayexpress