Genomic Sequencing of Lung Adenocarcinoma
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA157937 | ENA |
REPOSITORIES: ENA
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Project description:Methylation analysis of lung adenocarcinoma samples. Genomic DNA isolated directly from human lung adenocarcinoma specimens.
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Project description:<p>Lung carcinoma is the leading cause of cancer death in the United States and world-wide; lung adenocarcinoma is the most common cause of lung cancer. Pilot studies of lung adenocarcinoma with hybrid-capture based whole exome sequencing will enable us to identify new targets for therapy and improve diagnosis. We will analyze a blend of whole exome and whole genome sequencing data as well as copy number and somatic mutation calls for 200 tumor and matched normal controls. When completed this study will represent the most comprehensive lung adenocarcinoma genome dataset to date.</p>
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Project description:One of the most fertile applications of next generation sequencing will be in the field of cancer genomics. Here, we report a high-throughput multi-dimensional sequencing study of primary non-small cell lung adenocarcinoma tumors and adjacent normal tissues of 6 never-smoker Korean female patients. Our data encompass results from exome-seq, RNA-seq, small RNA-seq, and MeDIP-seq. We identified and validated novel genetic aberrations including 47 somatic mutations and 20 fusion transcripts. We also characterized gene expression profiles which we sought to integrate with genomic aberrations and epigenetic regulations into functional networks. Importantly, among others the gene network module governing G2/M cell check point emerged as the primary source of disturbance in these patients. In addition, our study strongly suggests that microRNAs make key regulatory inputs into this gene network module. Our study offers a paradigm for integrative genomics analysis and proposes potential target pathways for the control of non-small cell lung adenocarcinoma. Study of primary non-small cell lung adenocarcinoma tumors and normal tissues of 6 patients.
2013-05-10 | E-GEOD-37764 | biostudies-arrayexpress
Project description:MeRIP-sequencing in lung adenocarcinoma cells
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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:Genomic study of lung adenocarcinoma in young never-smokers
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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:We performed single cell RNA sequencing (scRNA-seq) for 208,506 cells derived from 58 lung adenocarcinomas from 44 patients, which covers primary tumour, lymph node and brain metastases, and pleural effusion in addition to normal lung tissues and lymph nodes. The extensive single cell profiles depicted a complex cellular atlas of lung adenocarcinoma progression which includes cancer, stromal, and immune cells in the surrounding tumor microenvironments.
2020-03-27 | GSE131907 | GEO
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:41 lung adenocarcinoma from never-smokers hybridized on Illumina SNP arrays on 13 HumanCNV370-Quadv3 chips. High-resolution array comparative genomic hybridization analysis of lung adenocarcinoma in 41 never smokers for identification of new minimal common regions (MCR) of gain or loss. The SNP array analysis validated copy-number aberrations and revealed that RB1 and WRN were altered by recurrent copy-neutral loss of heterozygosity.The present study has uncovered new aberrations containing cancer genes. The oncogene FUS is a candidate gene in the 16p region that is frequently gained in never smokers. Multiple genetic pathways defined by gains of MYC, deletions of RB1 and WRN or gains on 7p and 7q are involved in lung adenocarcinoma in never smokers. A 'Cartes d'Identite des Tumeurs' (CIT) project from the French National League Against Cancer (http://cit.ligue-cancer.net) 41 samples hybridized on Illumina SNP arrays. Submitter : Fabien PETEL petelf@ligue-cancer.net . Project leader : Pr Pierre FOURET pierre.fouret@psl.aphp.fr
2011-07-28 | E-TABM-1169 | biostudies-arrayexpress