D6e8c867-741a-40ec-888b-6e5df5004cad - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001008950 | EGA |
REPOSITORIES: EGA
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Project description:We conducted whole-exome sequencing (WES) and microarray profiling on 19 micro-dissected tumor regions of different histologic subtypes from 9 patients with lung cancers of mixed histologic patterns including 6 LUAD, 6 LCNEC, 3 SCLC, 3 LUSC, and one poorly differentiated NSCLC-NOS.
| EGAD00001007076 | EGA
Project description:Long noncoding RNAs (lncRNAs) are known to regulate the development and progression of various cancers, however, few lncRNAs have been well characterized in lung adenocarcinoma (LUAD). Understanding the expression profile of lncRNAs and protein-coding genes is critical to develop new diagnosis and treatment strategies for LUAD and improving the prognosis of diagnosed patients. Five female LUAD patients with no smoking history were selected to profile lncRNA and protein-coding gene expression with microarrays. Paired tumor tissues and adjacent nontumor tissues were collected and confirmed by pathologists.
2015-03-10 | E-GEOD-66654 | biostudies-arrayexpress
Project description:Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer and shows high morbidity and mortality rates as well as poor prognosis. However, there is still an urgent need to provide more effective biomarkers for the early diagnosis, prognosis and monitoring of LUAD. The Arraystar Human M6a-MRNA&lncRNA Epitranscriptomic microarray analysis was performed on six pairs of LUAD tissues and adjacent non-tumor tissues to compare and screen the M6a marker of LUAD, thus may offer a new avenue of targets and strategies for LUAD diagnosis and treatment.
2021-07-20 | GSE176348 | GEO
Project description:Lung cancer is the leading cause of cancer-related death in the United States. Long non-coding RNAs (lncRNAs) are a class of regulatory molecules whose role in lung carcinogenesis is poorly understood. In this study, we profiled lncRNA expression in lung adenocarcinoma (LUAD) cell lines, compared their expression to that of purified alveolar epithelial type II cells (the purported cell of origin for LUAD), cross-referenced these with lncRNAs altered in primary human tumors, and interrogated for lncRNA whose expression correlated with patient survival. We identified LINC00261, a lncRNA with unknown function in LUAD, adjacent to the pioneering transcription factor FOXA2. Loss of LINC00261 was observed in multiple tumor types, including liver, breast, and gastric cancer. Reintroduction of LINC00261 into human LUAD cell lines inhibited cell migration and slowed proliferation by inducing a G2/M cell cycle arrest while upregulating DNA damage pathway genes and inducing phosphorylation-mediated activation of components of the DNA damage pathway. FOXA2 was able to induce LINC00261 expression, and the entire locus underwent hypermethylation in LUAD, leading to loss of expression. We have thus identified an epigenetically deregulated lncRNA, whose loss of expression in LUAD promotes the malignant phenotype and blocks activation of the DNA damage machinery, predisposing lung cells to cancer development.
2019-03-01 | GSE110024 | GEO
Project description:Lung cancer is the leading cause of cancer-related death in the United States. Long non-coding RNAs (lncRNAs) are a class of regulatory molecules whose role in lung carcinogenesis is poorly understood. In this study, we profiled lncRNA expression in lung adenocarcinoma (LUAD) cell lines, compared their expression to that of purified alveolar epithelial type II cells (the purported cell of origin for LUAD), cross-referenced these with lncRNAs altered in primary human tumors, and interrogated for lncRNA whose expression correlated with patient survival. We identified LINC00261, a lncRNA with unknown function in LUAD, adjacent to the pioneering transcription factor FOXA2. Loss of LINC00261 was observed in multiple tumor types, including liver, breast, and gastric cancer. Reintroduction of LINC00261 into human LUAD cell lines inhibited cell migration and slowed proliferation by inducing a G2/M cell cycle arrest while upregulating DNA damage pathway genes and inducing phosphorylation-mediated activation of components of the DNA damage pathway. FOXA2 was able to induce LINC00261 expression, and the entire locus underwent hypermethylation in LUAD, leading to loss of expression. We have thus identified an epigenetically deregulated lncRNA, whose loss of expression in LUAD promotes the malignant phenotype and blocks activation of the DNA damage machinery, predisposing lung cells to cancer development.
2019-03-01 | GSE110182 | GEO
Project description:Lung adenocarcinoma (LUAD) is a high malignant tumor mostly occurs in adult patients, which is also a highly heterogeneous disease that involved multi different alterations. Some alterations such like EGFR mutations are frequently observed in LUAD patients, but the mechanisms that drive LUAD tumorigenesis and progression remain largely unclear, which need further researches. For example, epigenetic processes play important roles in cancers, but the variations in the enhancer and super enhancer landscapes of LUAD patients have rarely been studied. Here, to provide an in-depth understanding of the epigenomic heterogeneity of LUAD, we investigate the H3K27ac histone modification profiles of the tumor and adjacent normal lung tissues from 42 LUAD patients and explore the role of epigenetic alterations in LUAD progression.
2020-05-22 | GSE150975 | GEO
Project description:Lung adenocarcinoma (LUAD) is a high malignant tumor mostly occurs in adult patients, which is also a highly heterogeneous disease that involved multi different alterations. Some alterations such like EGFR mutations are frequently observed in LUAD patients, but the mechanisms that drive LUAD tumorigenesis and progression remain largely unclear, which need further researches. For example, epigenetic processes play important roles in cancers, but the variations in the enhancer and super enhancer landscapes of LUAD patients have rarely been studied. Here, to provide an in-depth understanding of the epigenomic heterogeneity of LUAD, we investigate the H3K27ac histone modification profiles of the tumor and adjacent normal lung tissues from 42 LUAD patients and explore the role of epigenetic alterations in LUAD progression.
2020-05-22 | GSE150976 | GEO
Project description:Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer and arises in the distal lung. LUAD encompasses several pathologic subtypes, including solid, lepidic, papillary, micropapillary, acinar and mixed subtypes, each with differing clinical outcomes or biological behavior. Specifically, lepidic histology is associated with improved survival relative to other LUAD histologies. Yet, the molecular and cellular underpinnings of these subtypes are largely unknown. Understanding which cell populations in the distal lung contribute to LUAD could provide insights for the marked heterogeneity in LUAD pathologic features, clinical presentation and responses to therapy.Recent studies have seen tumor-derived epithelial cells with an AT1 transcriptomic cell signature, suggesting AT1 cells may contribute to a subset of LUAD cases. We tested the ability of AT1 cells to give rise to LUAD by inducing KrasG12D, a known oncogenic driver in human LUAD. Activation of KrasG12D in Gram-domain containing 2 (Gramd2)+ AT1 cells gave rise to multiple LUAD lesions, primarily of papillary histology. In contrast, activation of KrasG12D in Sftpc+ AT2 cells resulted in LUAD lesions of lepidic histology. Immunohistochemistry established Gramd2:KrasG12D lesions were of primary lung origin and not metastatic events. Spatial transcriptomic profiling revealed distinct pathway alterations occurring within Gramd2- and Sftpc-derived LUAD. Immunofluorescence confirmed differences observed in the Spatial transcriptomic analysis in expression patterns and distribution of cell-specific markers between cell of origin, while universal upregulation of the Krt8 intermediate cell state marker was observed. Our results are consistent with Gramd2+ AT1 cells serving as a putative cell of origin for LUAD and suggest that LUAD may be a collection of adenocarcinomas that share a common location within the distal lung, but which arise from different cells of origin.
2022-10-19 | GSE215858 | GEO
Project description:To develop biomarkers for diagnosis of early-stage lung adenocarcinoma (LUAD) patients, we set up single-cell RNA sequencing (scRNA-seq) pipeline using Fluidigm C1 systems. Through the scRNA-seq pipeline, we clustered 1,441 single cells from four non-small cell lung cancer (NSCLC) cell lines (A549, H460, H1299 and Calu3) into four groups based on differential gene expression and detected over 2,400 differentially expressed genes (DEGs) from a comparison of four clusters following dimension reduction. We validated fold change values of 120 DEGs selected from three cluster comparisons (top 20 up- and top 20 down-regulated genes per cluster comparison) using qRT-PCR approach. We performed further quantitative validation of chemokine genes (CXCL1 and CXCL2 with corresponding receptor, CXCR2) at mRNA level in tumour and tumour-adjacent normal lung tissues of LUAD patients (16 female and 19 male). Next, we profiled microRNAs epigenetically regulating expression of those chemokine genes in the tumour and normal tissues as well as blood (plasma) samples from corresponding LUAD patients. Finally, we identified relatively high copy number of miR-532-5p regulating those chemokine genes in patient plasma samples.
2021-09-14 | GSE183590 | GEO
Project description:The expression of long non-coding RNAs - lncRNAs - was profiled in the lung adenocarcinoma patient samples (LUAD, Lu-T) and in normal lung tissues adjacent to tumors (Lu-N) using the Invitrogen NCode Human lncRNA Array Platform. will be published in: Anna Roth et al., Restoring LINC00673 expression triggers cellular senescence in lung cancer
2019-01-23 | GSE113852 | GEO