Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human lung adenocarcinoma DNA methylation profiling by MSNP

ABSTRACT: Lung adenocarcinoma’s genomic alterations exhibit vast variation. Lung adenocarcinoma also has previously described intrinsic gene expression subtypes (Hayes et al. 2006, PMID: 17075127). This study detect global methylation differences among gene expression subtypes. These specimens were also assayed for genomewide transcription in GSE26939 and copy number in GSE36363.

ORGANISM(S): Homo sapiens

PROVIDER: GSE36438 | GEO | 2012/05/17

SECONDARY ACCESSION(S): PRJNA155827

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Human lung adenocarcinoma DNA copy number profiling

2012-05-17 | GSE36363 | GEO

Human lung adenocarcinoma DNA methylation profiling by MSNP

Project description:Lung adenocarcinoma’s genomic alterations exhibit vast variation. Lung adenocarcinoma also has previously described intrinsic gene expression subtypes (Hayes et al. 2006, PMID: 17075127). This study detect global methylation differences among gene expression subtypes. These specimens were also assayed for genomewide transcription in GSE26939 and copy number in GSE36363. 33 tumor samples and 10 normal samples were quantified for DNA methylation by MSNP (Yuan et al, PMID: 16585166) using Affymetrix SNP 250K_StyI microarrays.

2012-05-16 | E-GEOD-36438 | biostudies-arrayexpress

Human lung adenocarcinoma DNA copy number profiling

Project description:Lung adenocarcinoma’s genomic alterations exhibit vast variation. Lung adenocarcinoma also has previously described intrinsic gene expression subtypes (Hayes et al. 2006, PMID: 17075127). This study’s aim was to detect and validate subtype-specific alterations. A portion of these specimens were also assayed for genomewide transcription in GSE26939. 103 tumor samples and 30 normal samples were quantified for DNA copy number using Affymetrix SNP microarrays.

2012-05-16 | E-GEOD-36363 | biostudies-arrayexpress

Expression data from Columbia Lung Adenocarcinoma Human Tumor Cells

Project description:The World Health Organization has subclassified adenocarcinoma based upon predominant cell morphology and growth pattern such as bronchioloalveolar carcinoma (BAC), adenocarcinoma with mixed subtypes (AC-mixed), and homogenously invasive tumors with a variety of histological patterns Pure invasive adenocarcinomas are often devoid of bronchioloalveolar morphology. The clinical importance of lung adenocarcinoma invasion is supported by several recent studies indicating that the risk of death in non-mucinous BAC is significantly lower than that of pure invasive tumors and in tumors with greater than 0.6 cm of fibrosis or linear invasion (J Thorac Oncol 6:244-285) To identify human tumor cell signatures associated with lung adenocarcinoma subtype and invasion, we performed microarray gene expression profiling of microdissected tumor cells noninvasive AC and AC-Mixed invasive tumors. 17 cases of noninvasive AC tumors and 23 cases of AC-mixed subtype invasive lung adenocarcinomas resected from 2002 to 2006 were examined (Columbia Lung Adenocarcinoma dataset)

2011-09-14 | E-GEOD-27716 | biostudies-arrayexpress

Gene expression differences between adenocarcinoma and squamous cell carcinoma in human NSCLC

2009-10-01 | GSE10245 | GEO

Human lung adenocarcinoma mRNA expression and gene mutations.

Project description:Lung adenocarcinoma expression subtypes have unknown origins. This study associated distinct mutations with the subtypes.

2012-05-17 | GSE26939 | GEO

Transcription profiling of human non-small cell lung cancer adenocarcinoma and squamous cell carcinoma subtypes

Project description:Non-small cell lung cancer (NSCLC) can be classified into the major subtypes adenocarcinoma (AC) and squamous cell carcinoma (SCC) subtypes. Although explicit molecular, histological and clinical characteristics have been reported for both subtypes, no specific therapy exists so far. However, the characterization of suitable molecular targets holds great promises to develop novel therapies in NSCLC. In the present study, global gene expression profiling of 58 human high grade NSCLC specimens revealed large transcriptomic differences between AC and SCC subtypes: More than 1.700 genes were found to be differentially expressed. Experiment Overall Design: The NSCLC patient collective was composed of the histological subtype adenocarcinoma (n=40) and squamous cell carcinoma (n=18). We subjected gene expression profiles of 40 AC and 18 SCC samples into further analysis. Unsupervised hierarchical clustering of all 58 NSCLC tumors using the 500 most variably expressed transcripts revealed two different clusters, which were strongly associated with the histological subtypes AC and SCC of NSCLC. Our result indicated that the major impact on global transcriptional changes was due to the NSCLC histology.

2009-10-11 | E-GEOD-10245 | biostudies-arrayexpress

Ito2019 - gefitnib resistance of lung adenocarcinoma caused by MET amplification

Project description:The model is based on publication: Mathematical analysis of gefitinib resistance of lung adenocarcinoma caused by MET amplification Abstract: Gefitinib, one of the tyrosine kinase inhibitors of epidermal growth factor receptor (EGFR), is effective for treating lung adenocarcinoma harboring EGFR mutation; but later, most cases acquire a resistance to gefitinib. One of the mechanisms conferring gefitinib resistance to lung adenocarcinoma is the amplification of the MET gene, which is observed in 5–22% of gefitinib-resistant tumors. A previous study suggested that MET amplification could cause gefitinib resistance by driving ErbB3-dependent activation of the PI3K pathway. In this study, we built a mathematical model of gefitinib resistance caused by MET amplification using lung adenocarcinoma HCC827-GR (gefitinib resistant) cells. The molecular reactions involved in gefitinib resistance consisted of dimerization and phosphorylation of three molecules, EGFR, ErbB3, and MET were described by a series of ordinary differential equations. To perform a computer simulation, we quantified each molecule on the cell surface using flow cytometry and estimated unknown parameters by dimensional analysis. Our simulation showed that the number of active ErbB3 molecules is around a hundred-fold smaller than that of active MET molecules. Limited contribution of ErbB3 in gefitinib resistance by MET amplification is also demonstrated using HCC827-GR cells in culture experiments. Our mathematical model provides a quantitative understanding of the molecular reactions underlying drug resistance.

2019-09-30 | BIOMD0000000827 | BioModels

Human lung adenocarcinoma NCI-H1975 cells: parental vs cell lines resistant to the EGFR-TK inhibitor CNX-2006

Project description:Genome variation profiling of lung adenocarcinoma cells comparing untreated NCI-H1975 cells with CNX-2006-resistant untreated cells. Goal was to determine the potential mechanism of resistance to mutant EGFR-TKIs and rationally design novel strategies for the treatment of EGFR-mutant lung cancer patients.

2015-07-01 | GSE53234 | GEO

miRNA sequence analysis of primary lesions, brain metastases, and normal lung tissues in lung adenocarcinoma

Project description:We obtained primary lesions, brain metastases, and normal lung tissues from lung adenocarcinoma patients. Next generation sequencing was performed to assess the expressions of miRNA in these specimens.

2023-04-26 | GSE230229 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data