CaArray_landi-00077: EAGLE Project
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE75324 | GEO | 2015/11/24
SECONDARY ACCESSION(S): PRJNA303191
REPOSITORIES: GEO
Similar Datasets
Project description:The EAGLE (Environmental and Genetic Lung Cancer Etiology) gene expression study is case-control study of lung cancer conducted in Milan, Italy, designed to identify molecular alteration, particularly gene expression variation induced by smoking in lung carcinoma in this data set. The study is initiated by the Division of Cancer Epidemiology and Genetics (DCEG). landi-00077 Assay Type: Gene Expression Provider: Affymetrix Array Designs: HG-U133A Organism: Homo sapiens (ncbitax) Material Types: synthetic_DNA, synthetic_RNA, total_RNA
2015-11-24 | E-GEOD-75324 | biostudies-arrayexpress
Project description:<p>The majority of cases of lung cancer are the culmination of a dynamic process that begins with smoking initiation, proceeds through dependency and smoking persistence, continues with lung cancer development and ends with progression to disseminated disease or response to therapy and survival. We are conducting a whole genome study of lung cancer and smoking to examine critical steps in lung cancer progression.</p> <p>This study is a genome-wide association study (GWAS) to investigate the genetic determinants of lung cancer risk. The study design efficiently allows identification of genes that also contribute to smoking persistence and outcome from lung cancer using a single GWAS of 5,900 subjects using the primary GENEVA dataset, derived from two studies. The first is the <b>E</b>nvironment <b>a</b>nd <b>G</b>enetics in <b>L</b>ung Cancer <b>E</b>tiology Study (EAGLE), a population-based, biologically intensive, case-control study from the Lombardy region of Italy including ~2000 newly diagnosed lung cancer cases and ~2000 age-, gender- and region- matched controls. The second is the <b>P</b>rostate, <b>L</b>ung, <b>C</b>olon and <b>O</b>vary Study (PLCO) Cancer Screening Trial from which we have selected ~850 lung cancer cases and ~850 controls, also matched on age and gender. Understanding the basis for the well-established hereditary component of lung cancer and smoking persistence could provide new insights into etiology, prevention, and treatment, and have an enormous impact on public health.</p> <p>The same GWAS genotyping data in the two studies will be used to investigate the genetic determinants of smoking persistence. Specifically, we will analyze current smokers and former smokers from EAGLE and PLCO for diverse smoking phenotypes, including persistence of smoking as well as ever/never smoking comparisons, quitting attempts, and the Fagerström index of tobacco addiction.</p> <p>PLCO participants are all European-Americans and EAGLE involves subjects from Italy.<br/> EAGLE is a case-control study and contains 3937 phenotyped subjects.<br/> PLCO is a screening trial with a cohort design and contains 1651 phenotyped subjects.</p> <p>This study is part of the Gene Environment Association Studies initiative (GENEVA, <a href="http://www.genevastudy.org" target="_blank">http://www.genevastudy.org</a>) funded by the trans-NIH Genes, Environment, and Health Initiative (GEI). The overarching goal is to identify novel genetic factors that contribute to lung cancer and smoking through large-scale genome-wide association studies of population-based samples of lung cancer cases and controls. Genotyping was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR). Data cleaning and harmonization were done at the GEI-funded GENEVA Coordinating Center at the University of Washington.</p>
| phs000093 | dbGaP
Project description:All cell lines were purchased from ATCC (LGC Standards S.r.l., Milan, Italy), except T-47D and MDA-MB-468 that were obtained from the National Cancer Institute Developmental Therapeutics Program (Frederick, MD).
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Project description:Scientific evidence indicates that genetic factors may contribute to differences in lung cancer risk for individuals with similar levels of tobacco exposure, which is the main environmental risk factor of lung cancer. Moreover, lung cancer patients show large differences in clinical staging and survival; these differences seem to be attributable, at least partially, to the genetic background. The analysis of the molecular properties (e.g., germline variations and genome-wide expression levels) of non-involved tissue from lung cancer patients may contribute in the identification of genetic factors involved in the development and progression of this pathology. To this aim, we analyzed two series (discovery series, n = 204, and validation series, n = 78) of non-tumor lung tissue samples from smokers that underwent surgical lobectomy for adenocarcinoma in Milan, Italy. First, we examined the whole transcriptome of these two series to define the candidate genes and pathways associated with either lung cancer risk or prognosis in this cohort. Moreover, as sex and age are known to strongly influence the pathophysiology of human lungs, we used transcriptome data from the same samples to identify sex- and age-related transcriptional differences in lung. Samples of non-involved (apparently normal) lung parenchyma excised from patients who underwent lobectomy for lung adenocarcinoma in the area around Milan, Italy. The samples were analyzed in two sets: a discovery series (n = 204) and a validation series (n = 78).
2016-01-20 | E-GEOD-71181 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of normal lung tissue samples. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs in nor mal lung tissue samples. Samples included 244 normal lung tissue samples from lung cancer patients. Environment and Genetics in Lung Cancer Etiology EAGLE; Population-based case-control study Bisulphite converted DNA from 244 fresh-frozen primary human lung samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip v1.2. This file has 60 samples.
2014-03-03 | E-GEOD-52401 | biostudies-arrayexpress
Project description:<p>The majority of cases of lung cancer are the culmination of a dynamic process that begins with smoking initiation, proceeds through dependency and smoking persistence, continues with lung cancer development and ends with progression to disseminated disease or response to therapy and survival. We are conducting a whole genome study of lung cancer and smoking to examine critical steps in lung cancer progression.</p> <p>This study is a genome-wide association study (GWAS) to investigate the genetic determinants of lung cancer risk. The study design efficiently allows identification of genes that also contribute to smoking persistence and outcome from lung cancer using a single GWAS of 5,900 subjects using the primary GENEVA dataset, derived from two studies. The first is the <b>E</b>nvironment <b>a</b>nd <b>G</b>enetics in <b>L</b>ung Cancer <b>E</b>tiology Study (EAGLE), a population-based, biologically intensive, case-control study from the Lombardy region of Italy including ~2000 newly diagnosed lung cancer cases and ~2000 age-, gender- and region- matched controls. The second is the <b>P</b>rostate, <b>L</b>ung, <b>C</b>olon and <b>O</b>vary Study (PLCO) Cancer Screening Trial from which we have selected ~850 lung cancer cases and ~850 controls, also matched on age and gender. Understanding the basis for the well-established hereditary component of lung cancer and smoking persistence could provide new insights into etiology, prevention, and treatment, and have an enormous impact on public health.</p> <p>The same GWAS genotyping data in the two studies will be used to investigate the genetic determinants of smoking persistence. Specifically, we will analyze current smokers and former smokers from EAGLE and PLCO for diverse smoking phenotypes, including persistence of smoking as well as ever/never smoking comparisons, quitting attempts, and the Fagerström index of tobacco addiction.</p> <p>PLCO participants are all European-Americans and EAGLE involves subjects from Italy.<br/> EAGLE is a case-control study and contains 3937 phenotyped subjects.<br/> PLCO is a screening trial with a cohort design and contains 1651 phenotyped subjects.</p> <p>This study is part of the Gene Environment Association Studies initiative (GENEVA, <a href="http://www.genevastudy.org" target="_blank">http://www.genevastudy.org</a>) funded by the trans-NIH Genes, Environment, and Health Initiative (GEI). The overarching goal is to identify novel genetic factors that contribute to lung cancer and smoking through large-scale genome-wide association studies of population-based samples of lung cancer cases and controls. Genotyping was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR). Data cleaning and harmonization were done at the GEI-funded GENEVA Coordinating Center at the University of Washington.</p>
| phs000093.v2.p2 | EGA
Project description:Smoking-associated DNA hypomethylation has been observed in blood cells and linked to lung cancer risk. However, its cause and mechanistic relationship to lung cancer remain unclear. We studied the association between tobacco smoking and epigenome-wide methylation in non-tumor lung (NTL) tissue from 237 lung cancer cases in the Environment And Genetics in Lung cancer Etiology study, using the Infinium HumanMethylation450 BeadChip. We identified seven smoking-associated hypomethylated CpGs (P < 1.0 × 10-7), which were replicated in NTL data from The Cancer Genome Atlas. Five of these loci were previously reported as hypomethylated in smokers' blood, suggesting that blood-based biomarkers can reflect changes in the target tissue for these loci. Four CpGs border sequences carrying aryl hydrocarbon receptor binding sites and enhancer-specific histone modifications in primary alveolar epithelium and A549 lung adenocarcinoma cells. A549 cell exposure to cigarette smoke condensate increased these enhancer marks significantly and stimulated expression of predicted target xenobiotic response-related genes AHRR (P = 1.13 × 10-62) and CYP1B1 (P < 2.49 × 10-61). Expression of both genes was linked to smoking-related transversion mutations in lung tumors. Thus, smoking-associated hypomethylation may be a consequence of enhancer activation, revealing environmentally-induced regulatory elements implicated in lung carcinogenesis
2018-02-07 | GSE94986 | GEO
Project description:Smoking-associated DNA hypomethylation has been observed in blood cells and linked to lung cancer risk. However, its cause and mechanistic relationship to lung cancer remain unclear. We studied the association between tobacco smoking and epigenome-wide methylation in non-tumor lung (NTL) tissue from 237 lung cancer cases in the Environment And Genetics in Lung cancer Etiology study, using the Infinium HumanMethylation450 BeadChip. We identified seven smoking-associated hypomethylated CpGs (P < 1.0 × 10-7), which were replicated in NTL data from The Cancer Genome Atlas. Five of these loci were previously reported as hypomethylated in smokers' blood, suggesting that blood-based biomarkers can reflect changes in the target tissue for these loci. Four CpGs border sequences carrying aryl hydrocarbon receptor binding sites and enhancer-specific histone modifications in primary alveolar epithelium and A549 lung adenocarcinoma cells. A549 cell exposure to cigarette smoke condensate increased these enhancer marks significantly and stimulated expression of predicted target xenobiotic response-related genes AHRR (P = 1.13 × 10-62) and CYP1B1 (P < 2.49 × 10-61). Expression of both genes was linked to smoking-related transversion mutations in lung tumors. Thus, smoking-associated hypomethylation may be a consequence of enhancer activation, revealing environmentally-induced regulatory elements implicated in lung carcinogenesis.
2018-02-07 | GSE69770 | GEO
Project description:All cell lines were purchased from ATCC (LGC Standards S.r.l., Milan, Italy), except T-47D and MDA-MB-468 that were obtained from the National Cancer Institute Developmental Therapeutics Program (Frederick, MD). Six untreated breast cancer cell lines grown according to the growth protocol reported below
2015-07-28 | E-GEOD-71395 | biostudies-arrayexpress
Project description:Scientific evidence indicates that genetic factors may contribute to differences in lung cancer risk for individuals with similar levels of tobacco exposure, which is the main environmental risk factor of lung cancer. Moreover, lung cancer patients show large differences in clinical staging and survival; these differences seem to be attributable, at least partially, to the genetic background. The analysis of the molecular properties (e.g., germline variations and genome-wide expression levels) of non-involved tissue from lung cancer patients may contribute in the identification of genetic factors involved in the development and progression of this pathology. To this aim, we analyzed two series (discovery series, n = 204, and validation series, n = 78) of non-tumor lung tissue samples from smokers that underwent surgical lobectomy for adenocarcinoma in Milan, Italy. First, we examined the whole transcriptome of these two series to define the candidate genes and pathways associated with either lung cancer risk or prognosis in this cohort. Moreover, as sex and age are known to strongly influence the pathophysiology of human lungs, we used transcriptome data from the same samples to identify sex- and age-related transcriptional differences in lung.
2016-01-20 | GSE71181 | GEO