Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA101605 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Chronic obstructive pulmonary disease (COPD) is an independent risk factor for lung cancer, suggesting that COPD stroma favors cancer initiation. Therefore, we used proteomics and polysome-profiling to identify gene expression programs that distinguish stroma of patients harboring lung cancer from those that do not, with varied COPD severities. This profiling unveiled distinct COPD-dependent cancer-associated gene expression programs predominantly manifesting as alterations in mRNA translation. Mechanistically, such programs are downstream of the mammalian target of rapamycin pathway in mild COPD and pathological extracellular matrix in more severe COPD; and both programs parallel activation of distinct pro-cancer fibroblast-derived secretomes. Therefore, depending upon COPD severity, the lung stroma can exist in two states favoring cancer initiation, which likely result in distinct disease entities.
2021-11-03 | PXD007743 | Pride
Project description:Background: CD8 cells seem to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, relatively little is known about their phenotype and function. Aims: To define the transcriptome of pulmonary CD8 cells in COPD and compare to paired circulating CD8 cells and smoker control pulmonary CD8 cells. COPD was defined according to the Global initiative for chronic Obstructive Lung Disease guidelines. Severity of disease was defined according to the patients lung function. In particular the forced evpiratroy volume in 1 second (FEV1).
2013-08-01 | E-MTAB-1688 | biostudies-arrayexpress
Project description:We profiled genome-wide gene expression in non-tumorous human lung tissues. The overall goal of this project is to improve our molecular understanding of various lung diseases including lung cancer and chronic obstructive pulmonary disease (COPD). The samples from the University of British Columbia (UBC) were derived from a long-standing tissue bank started by Drs. James C. Hogg and Peter D. Paré (Ding L, Quinlan KB, Elliott WM, Hamodat M, Paré PD, Hogg JC, Hayashi S. A Lung Tissue Bank for Gene Expression Studies in Chronic Obstructive Pulmonary Disease. COPD: Journal of Chronic Obstructive Pulmonary Disease 2004;1:191-204 (PMID 17136987)). Lung specimens were obtained from patients undergoing lung surgery. Primarily this was for resection of benign or malignant lesions. Some were the diseased lungs from transplant recipients. Patients are approached prior to surgery and asked if they would like to donate a portion of the lung tissue that is to be removed for research. It is explained that this would be done after the appropriate diagnostic specimens are taken and that only portions of lung that would be otherwise discarded will be used for research. A small number of lung samples were obtained at the time of autopsy. Immediately after resection, the lobes or lungs were inflated using a 50% mixture of Cryomatrix and saline. The specimens were then frozen in liquid nitrogen fumes and stored at -80C for later RNA extraction. RNAs were extracted and then hybridized to a single custom-made whole-genome human Affymetrix array.
2012-06-10 | E-GEOD-23529 | biostudies-arrayexpress
Project description:We profiled genome-wide gene expression in non-tumorous human lung tissues. The overall goal of this project is to improve our molecular understanding of various lung diseases including lung cancer and chronic obstructive pulmonary disease (COPD). Lung specimens were obtained from patients with a variety of lung diseases. After resection, tissue samples of the lobes or lungs not relevant for the diagnostic work-up were frozen and stored at -80C. RNAs were extracted and then hybridized to a single custom-made whole-genome human Affymetrix array.
2012-06-10 | E-GEOD-23545 | biostudies-arrayexpress
Project description:Alveolar epithelial type II (ATII) cells play a critical role in homeostasis and repair process of the lungs. In lung diseases such as chronic obstructive pulmonary disease (COPD), ATII cells are damaged and fall into apoptosis or senescence. Until to date, global gene expression of ATII cells in COPD lungs has not been analyzed. We isolated ATII cells from three non-COPD and three COPD patients using a FACS method. Then, we performed microarray analysis to compare gene expression profiles of ATII cells between non-COPD and COPD patients.
2012-10-11 | GSE29133 | GEO
Project description:Comparison of severely emphysematous tissue removed at lung volume reduction surgery to that of normal or mildly emphysematous lung tissue resected from smokers with nodules suspicious for lung cancer. Data obtained from the 18 patients with severe emphysema and 12 patients with mild/no emphysema. Research may provide insights into the pathogenetic mechanisms involved in chronic obstructive pulmonary disease (COPD).
2007-08-13 | E-GEOD-1650 | biostudies-arrayexpress
Project description:Epigenetics changes have been shown to be affected by cigarette smoking. It is possible that cigarette smoke (CS)-mediated DNA methylation would affect several cellular and pathophysiological processes, acute exacerbations, and comorbidity in lungs of patients with chronic obstructive pulmonary disease (COPD). We sought to determine whether genome-wide lung DNA methylation profiles of smokers and patients with COPD were significantly different from non-smokers. We isolated DNA from lung tissues of patients including 8 lifelong non-smokers, 8 current smokers, and 8 patients with COPD, and subsequently analyzed the samples using the Illumina’s Infinium HumanMethylation450 BeadChip.
2017-06-12 | GSE92511 | GEO
Project description:The objective is to establish robust transcriptional regulation differences between lung cancer (LC) and chronic obstructive pulmonary disease (COPD) by studying miRNA and concurrent transcriptional profiles
2014-07-03 | GSE44531 | GEO
Project description:Chronic obstructive pulmonary disease (COPD) is a progressive and irreversible chronic inflammatory lung disease. The abnormal inflammatory response of the lung, mainly to cigarette smoke, causes multiple cellular and structural changes affecting all of its compartments, which leads to disease progression. The molecular mechanisms underlying these pathological changes are still not fully understood The aim of this study was to identify genes and molecular pathways potentially involved in the pathogenesis of COPD Peripheral lung tissue samples from moderate COPD patients, smokers and nonsmokers were obtained. All patients were undergoing lung resection for localized carcinomas. RNA was extracted and processed for further hybridization on Affymetrix microarrays
2016-08-25 | E-GEOD-37768 | biostudies-arrayexpress
Project description:Chronic obstructive pulmonary disease (COPD) is a known risk factor for developing lung cancer suggesting that the COPD stroma contains factors supporting tumorigenesis. Since cancer initiation is complex we used a multi-omic approach to identify gene expression patterns that distinguish COPD stroma in patients with or without lung cancer. Our overall objective is the identification of gene expression pathways and levels of regulation in lung stroma of patients with COPD that harbor lung cancer. We obtained lung tissue from patients with COPD and lung cancer (tumor and adjacent non-malignant tissue) and those with COPD without lung cancer for proteomic and mRNA (cytoplasmic and polyribosomal) profiling. We used the joint and individual variation explained (JIVE) method to integrate and analysis across the three datasets. JIVE identified eight latent patterns that robustly distinguished and separated the three groups of tissue samples. Predictive variables that associated with the tumor, compared to adjacent stroma, were mainly represented in the transcriptomic data, whereas, predictive variables associated with adjacent tissue compared to controls was represented at the translatomic level. Kyoto Encyclopedia of Genes and Genome (KEGG) pathway analysis revealed extracellular matrix (ECM) and PI3K-Akt signaling pathways as important signals in the pre-malignant stroma. COPD stroma adjacent to lung cancer is unique and differs from non-malignant COPD tissue and is distinguished by the extracellular matrix and PI3K-Akt signaling pathways.
2019-05-28 | PXD007919 | Pride