Integrative analysis of lung adenocarcinoma in EAGLE (phase 2)
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ABSTRACT:
PROVIDER: PRJNA352760 | ENA |
REPOSITORIES: ENA
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Project description:Integrative analysis of lung adenocarcinoma in EAGLE
| PRJNA329162 | ENA
Project description:Integrative analysis of lung adenocarcinoma in EAGLE (phase 2)
| PRJNA352761 | ENA
Project description:<p>We performed an integrative genomic analysis, incorporating whole exome sequence, DNA copy number, DNA methylation and transcriptome sequencing, for 101 LUAD samples from the Environment And Genetics in Lung cancer Etiology (EAGLE) study.</p>
| phs001169 | dbGaP
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).
2015-11-24 | GSE75324 | GEO
Project description:Integrative analysis of lung adenocarcinoma in EAGLE
| PRJNA329163 | ENA
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
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:We have examined the both miRNA and mRNA expression profiles in 155 lung adenocarcinoma samples with known EGFR mutation status (52 mutated and 103 wild-type cases). An integrative analysis was performed to identify the unique miRNA-mRNA regulatory network in EGFR-mutated lung adenocarcinoma.
2018-11-13 | GSE119268 | GEO
Project description:We have examined the both miRNA and mRNA expression profiles in 155 lung adenocarcinoma samples with known EGFR mutation status (52 mutated and 103 wild-type cases). An integrative analysis was performed to identify the unique miRNA-mRNA regulatory network in EGFR-mutated lung adenocarcinoma.
2018-11-13 | GSE119267 | GEO
Project description:Genomic studies of lung adenocarcinoma (LUAD) have advanced understanding of the disease’s biology and accelerated targeted therapy. However, proteomic characteristics of LUAD remain poorly understood. We carried out comprehensive proteomic analysis of 103 cases of LUAD in Chinese patients. Integrative analysis of proteome, phosphoproteome, transcriptome, and whole-exome sequencing data revealed cancer associated characteristics, such as tumor-associated protein variants, distinct proteomic features, and clinical outcomes in patients of early stage or with EGFR and TP53 mutations. Proteome-based stratification of LUAD revealed three subtypes (S-I, S-II, S-III) related to different clinical and molecular features. Further, we nominated potential drug targets and validated the plasma protein level of HSP 90β as a potential prognostic biomarker for LUAD in an independent cohort. Our integrative proteomic analysis gives a more comprehensive understanding on the molecular landscape of LUAD and offers the opportunity for more precise diagnosis and treatment.
2020-07-10 | PXD020252 |