Lung adenocarcinoma cell line Wnt responsive signature
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE14107 | GEO | 2009/07/10
SECONDARY ACCESSION(S): PRJNA111197
REPOSITORIES: GEO
Similar Datasets
Project description:Identify Wnt3A responsive signature in lung adenocarcinoma cells Experiment Overall Design: 4 different cell lines +/- Wnt3A; replicate samples
2009-07-19 | E-GEOD-14107 | biostudies-arrayexpress
Project description:Identify Wnt3A responsive signature in lung adenocarcinoma cells Experiment Overall Design: 4 different cell lines +/- Wnt3A; replicate samples
| S-ECPF-GEOD-14107 | biostudies-other
Project description:Gene signature driving invasive mucinous adenocarcinoma of the lung
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Project description:Lung cancer remains the leading cause of cancer death worldwide. Overall 5-year survival is about 10-15% and despite curative intent surgery, treatment failure is primarily due to recurrent disease. Conventional prognostic markers are unable to determine which patients with completely resected disease within each stage group are likely to relapse. To identify a gene signature associated with recurrent adenocarcinoma (AC) of lung, we analyzed primary tumour gene expression for a total of 48 stage I ACs on 22,323 element microarrays, comparing expression profiles for individuals who remained disease-free for a minimum of 36 months with those from individuals whose disease recurred within 18 months of complete resection. Genome-wide profiling has revealed a distinct gene expression profile for recurrent lung AC which may be clinically useful as a prognostic tool. Keywords: non-small cell lung carcinoma, squamous cell, tumor recurrence, expression profiling
2007-05-01 | GSE5843 | GEO
Project description:Background: The occurrence of lung adenocarcinoma (LUAD) is a complicated process, involving the genetic and epigenetic changes of proto-oncogenes and oncogenes. The objective of this study was to establish new predictive signatures of lung adenocarcinoma based on copy number variation (CNVs) and gene expression data. Methods: Next-generation sequencing was implemented to obtain gene expression and CNV information. According to univariate, multivariate survival Cox regression analysis and Lasso analysis, the expression profiles of lung adenocarcinoma patients were screened and a risk score formula was established and experimentally validated in a local cohort. The model was evaluated by three independent cohorts, and then validated by clinical samples from LUAD patients. Results: A total of 844 CNV-related differential expressed genes (CNV related DEGs) were identified. An CNV associated-six gene signature was dramatically linked to overall survival in lung adenocarcinoma samples from both training and validation groups. Functional enrichment analysis further revealed involvement of genes in p53 signaling pathway and cell cycle, as well as the mismatch repair pathway. Risk score is an independent marker considering clinical parameters and had better prediction in clinical sub-population. The same signature also classified tumors tissues of clinical patients those with CNV detected from their corresponding non-tumorous tissues with an accuracy of 0.92. Conclusions: In conclusion, we identified a new class of 6 CNV-related gene markers that may act as efficient prognostic predictors of lung adenocarcinoma, thus contributing to individualized treatment decisions in patients.
2022-10-26 | GSE197346 | GEO
Project description:Primary dermal fibroblasts from patients with dSSc and healthy controls were treated with TGF beta for up to 24h and the genome-wide patterns of gene expression measured on DNA microarrays. 894 genes were identified as TGF beta-responsive in 4 independent cultures of dermal fibroblasts (2 healthy control and 2 dSSc patients). The 894 genes in the TGF beta-responsive signature are associated with induction of growth factor signaling, collagen synthesis and extracellular matrix deposition.
2009-09-15 | GSE12493 | GEO
Project description:The NKX2-1 transcription factor, a regulator of normal lung development, is the most significantly amplified gene in human lung adenocarcinoma. To better understand how genomic alterations of NKX2-1 drive tumorigenesis, we generated an expression signature associated with NKX2-1 amplification in human lung adenocarcinoma, and analyzed DNA binding sites of NKX2-1 by genome-wide chromatin immunoprecipitation from NKX2-1-amplified human lung adenocarcinoma cell lines. Combining these expression and cistromic analyses identified LMO3, itself encoding a transcription regulator, as a candidate direct transcriptional target of NKX2-1, in addition to consensus binding motifs including a nuclear hormone receptor signature and a Forkhead box motif in NKX2-1-bound sequences. RNA interference analysis of NKX2-1-amplified cells compared to non-amplified cells demonstrated that LMO3 mediates cell proliferation downstream of NKX2-1; cistromic analysis that NKX2-1 may cooperate with FOXA1. Our findings provide new insight into the transcriptional regulatory network of NKX2-1 and suggest that LMO3 is a transducer of lineage specific cell survival of NKX2-1-amplified lung adenocarcinomas. NKX2-1 ChIP-seq from three lung adenocarcinoma cell lines with amplification of NKX2-1
2013-01-22 | E-GEOD-39998 | biostudies-arrayexpress
Project description:FVB, Balb/c, and C57BL/6 mice received the tobacco carcinogens urethane (Sigma Aldrich, U2500) intraperitoneally (1g/Kg in 100 μl phosphate-buffered saline) or diethylnitrosamine (200 mg/kg) (Sigma Aldrich, N0756). Carcinogen induced lung adenocarcinoma murine cell lines generation| Ten months post first carcinogen (urethane, DEN) exposure mice were sacrificed, lung tumours were dissected from surrounding healthy lung parenchyma under sterile conditions, were halved, one half was processed for histology and the other half was chopped into 1 mm pieces and seeded to cell culture dishes. Cells were cultured under standard conditions outlined below. When adenocarcinoma was diagnosed for a given tumour, its corresponding culture was passaged in vitro over a period of 18 months and 60 passages, whichever occurred first. After gene expression and mutational signature extraction, the signature were compared with human lung adenocarcinoma RNAseq results.
2022-10-24 | GSE126119 | GEO
Project description:It has been well-known that cancer cells acquire approximately three-fold radioresistance under hypoxia than under normoxia due to both radiation chemical and radiation biological mechanisms, causing a negative impact on the outcome of radiation therapy. In the present study, to identify genes responsive to hypoxia in human cervical epithelial adenocarcinoma HeLa cells, global-scale gene expression analysis was carried out using a GeneChip® system.
2020-11-13 | GSE161393 | GEO
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