Non-small-cell lung tumor and normal lung tissue methylation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE27902 | GEO | 2012/07/03
SECONDARY ACCESSION(S): PRJNA138213
REPOSITORIES: GEO
Similar Datasets
Project description:Using paired tumor and non-tumor lung tissues from 47 individuals we identified common changes in DNA methylation associated with the development of non-small cell lung cancer. Pathologically normal lung tissue taken at the time of cancer resection was matched to tumorous lung tissue and together were probed for methylation status using Illumina GoldenGate arrays. For each matched pair the change in methylation at each CpG was calculated (the odds ratio), and these ratios were averaged across individuals and ranked by magnitude to identify the CpGM-bM-^@M-^Ys with the greatest change in methylation associated with tumor development. Using paired tumor and non-tumor lung tissues from 47 individuals we identified common changes in DNA methylation associated with the development of non-small cell lung cancer. Pathologically normal lung tissue taken at the time of cancer resection was matched to tumorous lung tissue and together were probed for methylation status using Illumina GoldenGate arrays. For each matched pair the change in methylation at each CpG was calculated (the odds ratio), and these ratios were averaged across individuals and ranked by magnitude to identify the CpGM-bM-^@M-^Ys with the greatest change in methylation associated with tumor development.
2012-07-02 | E-GEOD-27902 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE32861: Genome-scale analysis of DNA methylation in lung adenocarcinoma and integration with mRNA expression GSE32863: Gene expression analysis of lung adenocarcinoma and matched adjacent non-tumor lung tissue GSE32866: Genome-scale DNA methylation profiling of lung adenocarcinoma: validation using Ontario Tumor Bank samples Refer to individual Series
2012-03-21 | E-GEOD-32867 | biostudies-arrayexpress
Project description:Gene expression profiling of 60 lung adenocarcinoma tumors and their matched histologically normal adjacent lung tissue samples were analyzed using Illumina HumanWG-6 v3.0 expression beadchip. We integrated these data with DNA methylation profiles of the same samples to identify potential DNA methylation regulated genes. Lung cancer is the leading cause of cancer death worldwide and adenocarcinoma is its most common histological subtype. Clinical and molecular evidence indicates that lung adenocarcinoma is a heterogeneous disease, which has important implications for treatment. Here we performed genome-scale DNA methylation profiling using the Illumina Infinium HumanMethylation27 platform on 59 matched lung adenocarcinoma/non-tumor lung samples, with genome-scale verification on an independent set of tissues. We identified 766 genes showing altered DNA methylation between tumors and non-tumor lung. By integrating DNA methylation and mRNA expression data, we identified 164 hypermethylated genes showing concurrent downregulation, and 57 hypomethylated genes showing increased expression. Integrated pathways analysis indicates that these genes are involved in cell differentiation, epithelial to mesenchymal transition, RAS and WNT signaling pathways and cell cycle regulation, among others. Comparison of DNA methylation profiles between lung adenocarcinomas of current and never-smokers showed modest differences, identifying only LGALS4 as significantly hypermethylated and downregulated in smokers. LGALS4, encoding a galactoside-binding protein involved in cell-cell and cell-matrix interactions, was recently shown to be a tumor-suppressor in colorectal cancer. Unsupervised analysis of the DNA methylation data identified two tumor subgroups, one of which showed increased DNA methylation and was significantly associated with KRAS mutation and to a lesser extent, with smoking. Our analysis lays the groundwork for further molecular studies of lung adenocarcinoma by providing new candidate DNA methylation biomarkers for early detection, identifying novel molecular alterations potentially involved in lung adenocarcinoma development/progression, and describing an epigenetic subgroup of lung adenocarcinoma associated with KRAS mutation. 58 lung adenocarcinoma and 58 adjacent non-tumor lung fresh frozen tissues were macrodissected, and total RNA was isolated to be analyzed using the Illumina HumanWG-6 v3.0 expression beadchip.
2012-03-21 | E-GEOD-32863 | biostudies-arrayexpress
Project description:The Illumina GoldenGate® methylation array was used to evaluate DNA methylation at 1,505 CpG sites in 807 cancer-related genes in 91 consecutive CRC samples and 28 matched normal colonic mucosa. Bisulphite converted DNA from the 119 samples (91 CRC, 28 matched normals) were hybridised to the Illumina GoldenGate® methylation array.
2012-07-17 | E-GEOD-39446 | biostudies-arrayexpress
Project description:The Illumina GoldenGate® methylation array was used to evaluate DNA methylation at 1,505 CpG sites in 807 cancer-related genes in 91 consecutive CRC samples and 28 matched normal colonic mucosa.
2012-07-18 | GSE39446 | GEO
Project description:Gene expression profiling of 60 lung adenocarcinoma tumors and their matched histologically normal adjacent lung tissue samples were analyzed using Illumina HumanWG-6 v3.0 expression beadchip. We integrated these data with DNA methylation profiles of the same samples to identify potential DNA methylation regulated genes. Lung cancer is the leading cause of cancer death worldwide and adenocarcinoma is its most common histological subtype. Clinical and molecular evidence indicates that lung adenocarcinoma is a heterogeneous disease, which has important implications for treatment. Here we performed genome-scale DNA methylation profiling using the Illumina Infinium HumanMethylation27 platform on 59 matched lung adenocarcinoma/non-tumor lung samples, with genome-scale verification on an independent set of tissues. We identified 766 genes showing altered DNA methylation between tumors and non-tumor lung. By integrating DNA methylation and mRNA expression data, we identified 164 hypermethylated genes showing concurrent downregulation, and 57 hypomethylated genes showing increased expression. Integrated pathways analysis indicates that these genes are involved in cell differentiation, epithelial to mesenchymal transition, RAS and WNT signaling pathways and cell cycle regulation, among others. Comparison of DNA methylation profiles between lung adenocarcinomas of current and never-smokers showed modest differences, identifying only LGALS4 as significantly hypermethylated and downregulated in smokers. LGALS4, encoding a galactoside-binding protein involved in cell-cell and cell-matrix interactions, was recently shown to be a tumor-suppressor in colorectal cancer. Unsupervised analysis of the DNA methylation data identified two tumor subgroups, one of which showed increased DNA methylation and was significantly associated with KRAS mutation and to a lesser extent, with smoking. Our analysis lays the groundwork for further molecular studies of lung adenocarcinoma by providing new candidate DNA methylation biomarkers for early detection, identifying novel molecular alterations potentially involved in lung adenocarcinoma development/progression, and describing an epigenetic subgroup of lung adenocarcinoma associated with KRAS mutation.
2012-03-21 | GSE32863 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE23352: Whole-genome gene expression profiles of non-tumorous human lung tissues: Laval set GSE23529: Whole-genome gene expression profiles of non-tumorous human lung tissues: UBC set GSE23545: Whole-genome gene expression profiles of non-tumorous human lung tissues: GRNG set Refer to individual Series
2012-06-10 | E-GEOD-23546 | biostudies-arrayexpress
Project description:Tumor heterogeneity is a major barrier to effective cancer diagnosis and treatment. We recently identified cancer-specific differentially DNA-methylated regions (cDMRs) in colon cancer, which also distinguish normal tissue types from each other. We therefore hypothesized that these colon cDMRs might also be cDMRs for other cancer types. For colon, lung, breast, thyroid, and Wilms tumors, we show stochastic variation in methylation within each tumor type, but involving the same loci across tumor types, with intermediate values of variation for premalignant adenomas. Seeking to increase the precision of DNA methylation measurements over our previous tiling array-based approach, termed CHARM (Comprehensive High-throughput Array for Relative Methylation), we designed a custom nucleotide-specific bead array on the Illumina GoldenGate platform to analyze 151 colon cDMRs from Irizarry et al. (PMID 19151715). The resulting 384 probes covered 139 regions, with 1-7 probes per region. We studied 290 samples, including cancers from colon (10), lung (24), breast (27), thyroid (36), and kidney (Wilms) (25), with matched normal tissues to 111 of these 122 cancers, along with 30 colon premalignant adenomas, 18 normal colon, and 9 normal breast samples.
2011-06-01 | E-GEOD-29505 | biostudies-arrayexpress
Project description:DNA methylation profiling of lung adenocarcinomas and patient-matched non-malignant lung
| PRJNA578118 | ENA
Project description:Lung adenocarcinoma (ADC) is the most prevalent subtype of lung cancer and characterized by considerable morphological and mutational heterogeneity. However, little is known about the epigenomic intratumor variability between spatially separated histological growth patterns of ADC. In order to reconstruct the clonal evolution of histomorphological growth patterns, we performed global DNA methylation profiling of 27 primary tumor regions, seven matched normal tissues, and six lymph node metastases from seven ADC cases. Additionally, we investigated the methylation data from 369 samples of the TCGA ADC cohort. All regions showed varying degrees of methylation changes between segments of different, but also of the same growth patterns. Similarly, copy number variations were seen between spatially distinct segments of each patient. Hierarchical clustering of promoter methylation revealed extensive heterogeneity within and between the cases. Intra-tumor DNA methylation heterogeneity demonstrated a branched clonal evolution of ADC regions driven by genomic instability with subclonal copy number changes. Notably, methylation profiles within tumors were not more similar to each other than to those from other individuals. In two cases, different tumor regions of the same individuals were represented in distant clusters of the TCGA cohort, illustrating the extensive epigenomic intratumor heterogeneity of ADCs. Importantly, we found no evidence for the lymph node metastases to be derived from a common growth pattern. Instead, they had evolved early and separately from a particular pattern in each individual primary tumor. In summary, our results suggest that extensive variation of epigenomic features contributes to the molecular and phenotypic heterogeneity of primary ADCs and lymph node metastases.
2019-05-15 | GSE114989 | GEO