Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic profiling of lung adenocarcinoma associated alleles in A549s

ABSTRACT: Transcriptomic profiling of lung adenocarcinoma associated alleles in A549s

PROVIDER: PRJNA855953 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19991300_1.fastq.gz	Fastqsanger.gz
	SRR19991300_2.fastq.gz	Fastqsanger.gz
	SRR19991400_1.fastq.gz	Fastqsanger.gz
	SRR19991400_2.fastq.gz	Fastqsanger.gz
	SRR19991500_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 2472

Similar Datasets

Transcriptomic profiling of lung adenocarcinoma associated alleles in A549s

Project description:Based on the previous eVIP study (Cancer Cell, 2016), we profiled the transcriptomes of lung adenocarcinoma cell lines expressing oncogenes to compare methods and investigate the effects of these oncogenes on the cells' whole transcriptomes, differential expression, and alternative splicing

2022-07-10 | GSE207511 | GEO

Transcriptomic profiling of Lung adenocarcinoma brain metastasis

Project description:Transcriptomic profiling of Lung adenocarcinoma brain metastasis

| PRJNA594359 | ENA

Gene expression from mouse lung adenocarcinoma-associated macrophages

Project description:Gene expression from mouse lung adenocarcinoma-associated macrophages

| PRJNA471545 | ENA

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.

2024-09-02 | BIOMD0000000827 | BioModels

Transcriptomic profiling of lung adenocarcinoma from never-smokers

Project description:Transcriptomic profiling of lung adenocarcinoma from never-smokers

| PRJNA1231614 | ENA

Transcriptomic profiling of lung adenocarcinoma from never-smokers

Project description:Transcriptomic profiling of lung adenocarcinoma from never-smokers

| PRJNA1231615 | ENA

Transcriptomic profiling of Lung adenocarcinoma brain metastasis

Project description:Brain metastasis developed in nearly 40% of lung adenocarcinoma (LUAD) patients diagnosed with distant metastasis. There is lack of transcriptomic data of brain lesions from human lung adenocarcinoma patients. As part of the project to understanding the tumor microenvironment in brain metastasis of LUAD patients, we performed bulk RNA analysis on brain metastases from 6 LUAD patients. In order to understand the tumor intrinsic factors that potential shape the tumor microenvironment, we compared these data with bulk RNA sequencing data from 14 early stage and 11 late stage primary LUAD tumor from TCGA database. Pathway expression analysis showed a downregulation of pro-inflammatory signals in brain metastasis and upregulation of DNA synthesis and oxidative phosphorylation pathways related to rapid proliferation in brain lesions.

2019-12-10 | GSE141685 | GEO

Gene expression from mouse lung adenocarcinoma-associated macrophages

Project description:Comparison of gene expression of mouse lung adenocarcinoma-associated macrophages isolated from C57BL/6 mice injected with Kras-CL and Kras IKKa low cells

2018-05-16 | GSE114501 | GEO

Transcriptomic analyses of lung adenocarcinoma cells

Project description:Transcriptomic analyses of lung adenocarcinoma cells

| PRJNA843347 | ENA

Single-cell analyis of tobacco-associated lung adenocarcinoma development

Project description:Single-cell analyis of tobacco-associated lung adenocarcinoma development

| PRJNA923805 | ENA