Multi-region exome sequencing of lung adenocarcinoma precursors -1
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ABSTRACT:
PROVIDER: EGAS00001003439 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Clinical FFPE tissue proteomic analyses were performed for early lung adenocarcinomas including adenocarcinoma in-situ (AIS), minimally invasive adenocarcinoma (MIA) and lepidic predominant invasive adenocarcinoma (LPA).
2020-01-30 | PXD017334 | JPOST Repository
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
Project description:Invasive subtypes of lung adenocarcinoma (LUAD) show MDM2 amplification that is associated with poor survival. Mouse double minute 2 (MDM2) is frequently amplified in lung adenocarcinoma (LUAD) and is a negative regulator of p53, which binds to p53 and regulates its activity and stability. Genomic amplification and overexpression of MDM2 together with genetic alterations in p53 leads to genomic and genetic heterogeneity in LUAD that represents a therapeutic target. In vitro assays in a panel of LUAD cell lines showed that tumor cell response to MDM2 targeted therapy is associated with MDM2 amplification.
2022-12-31 | GSE191171 | GEO
Project description:Lung adenocarcinoma is the most common histologic subtype of non-small cell lung cancer. There exists a need to identify new molecular regulators for lung adenocarcinoma, providing insights into potential therapeutic targets. We used microarrays to identify up-regulated genes in invasive lung adenocarcinoma.
2019-01-23 | GSE118370 | GEO
Project description:Intercepting progression from pre-invasive to invasive lung adenocarcinoma
| PRJNA808146 | ENA
Project description:Intercepting progression from pre-invasive to invasive lung adenocarcinoma
| PRJNA808147 | ENA
Project description:Bronchioloalveolar carcinoma (BAC), a subtype of lung adenocarcinoma (ADC) without stromal, vascular, or pleural invasion, is considered an in situ tumor with a 100% survival rate. However, the histological criteria for invasion remain controversial. BAC-like areas may accompany otherwise invasive adenocarcinoma, referred to as mixed type adenocarcinoma with BAC features (AWBF). AWBF are considered to evolve from BAC, representing a paradigm for malignant progression in ADC. However, the supporting molecular evidence remains forthcoming. Here, we have studied the genomic changes of BAC and AWBF by array comparative genomic hybridization (CGH). We used submegabase-resolution tiling set array CGH to compare the genomic profiles of 14 BAC or BAC with focal area suspicious for invasion with those of 15 AWBF. Threshold-filtering and frequency-scoring analysis found that genomic profiles of noninvasive and focally invasive BAC are indistinguishable and show fewer aberrations than tumor cells in BAC-like areas of AWBF. These aberrations occurred mainly at the subtelomeric chromosomal regions. Increased genomic alterations were noted between BAC-like and invasive areas of AWBF. We identified 113 genes that best differentiated BAC from AWBF and were considered candidate marker genes for tumor invasion and progression. Correlative gene expression analyses demonstrated a high percentage of them to be poor prognosis markers in early stage ADC. Quantitative PCR also validated the amplification and overexpression of PDCD6 and TERT on chromosome 5p and the prognostic significance of PDCD6 in early stage ADC patients. We identified candidate genes that may be responsible for and are potential markers for malignant progression in AWBF. Keywords: array comparitive genomic hybridization, bronchioloalveolar carcinoma, non-small-cell lung carcinoma, prognostic markers Array comparitive genomic hybridization analysis of 29 Lung Adenocarcinomas with Bronchioalveolar Features.
2008-07-01 | E-GEOD-11945 | biostudies-arrayexpress
Project description:Genome wide DNA methylation profiling of Stage I Lung Adenocarcinoma and non-tumor adjacent tissues. The Illumina Infinium 27k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 27,000 CpGs. Samples included tumor and adjacent non-tumor tissues excised from a cohort of 35 patients with Stage I Lung Adenocarcinoma. Candidate prognostic biomarkers were validated by pyrosequencing in independent cohorts. Total genomic DNA was bisulfite converted and hybridized to Infinium Human Methylation27Beadchips. Fluorescent signals were collated via Bead Studio software and converted into β-values. Illumina Bead Studio software output data were normalized using SSN (simple scaling normalization), to correct for dye bias and transformed into M-values (M = log2 intensity of methylated probe/ intensity of unmethylated probe), using the R package lumi.
2015-04-30 | E-GEOD-63384 | biostudies-arrayexpress
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 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.
2011-09-15 | GSE27716 | GEO