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Unique microRNA profiles in EGFR-mutated lung adenocarcinomas

ABSTRACT: We have examined the microRNA expression in 154 lung adenocarcinoma samples and 20 paired normal lung tissue samples and investigated the microRNA expression to clinical variables, EGFR- and KRAS- mutational status and time to progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE48414 | GEO | 2014/03/10

SECONDARY ACCESSION(S): PRJNA209985

REPOSITORIES: GEO

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Unique microRNA profiles in EGFR-mutated lung adenocarcinomas

Project description:We have examined the microRNA expression in 154 lung adenocarcinoma samples and 20 paired normal lung tissue samples and investigated the microRNA expression to clinical variables, EGFR- and KRAS- mutational status and time to progression. 174 samples are analyzed. 154 from lung adenocarcinoma tumor tissue and 20 from paired normal lung tissue samples. No replicates or control samples included.

2014-03-10 | E-GEOD-48414 | biostudies-arrayexpress

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Analysis of miRNA expression profiling in 3 samples(normal, cigarette smoking and lung cancer population's serum)

Project description:Using the highly sensitive miRNA array, we determined the serum miRNAs profiles of 10 non-smokers, 10 smokers and 10 lung cancer patients by miRCURY LNA™ microRNA Arrays. Differential expressed miRNAs were further validated in a larger scale samples. We found that let-7i-3p and miR-154-5p were significantly downregulation in serum of smokers and lung cancer patients. The serum level of let-7i-3p and miR-154-5p is associated with smoking and smoking-related lung cancer.

2014-06-17 | GSE58540 | GEO

Proteogenomic systems analysis identifies targeted therapy resistance mechanisms in EGFR-mutated lung cancer

Project description:Cancer precision medicine largely relies on knowledge about genetic aberrations in tumors and next-generation-sequencing studies have shown a high mutational complexity in many cancers. Although a large number of the observed mutations is believed to be not causally linked with cancer, the functional effects of many rare mutations but also of combinations of driver mutations are often unknown. Here, we perform a systems analysis of a model of EGFR-mutated non-small cell lung cancer resistant to targeted therapy that integrates whole exome sequencing, global time-course discovery phosphoproteomics and computational modeling to identify functionally relevant molecular alterations. Our approach allows for a complexity reduction from over 2,000 genetic events potentially involved in mediating resistance to only 44 phosphoproteins and 35 topologically close genetic alterations. We perform single- and combination-drug testing against the predicted phosphoproteins and discovered that targeting of HSPB1, DBNL and AKT1 showed potent anti-proliferative effects overcoming resistance against EGFR-inhibitory therapy. Our approach may therefore be used to complement mutational profiling to identify functionally relevant molecular aberrations and propose combination therapies across cancers.

2018-07-02 | PXD009996 | Pride

MicroRNA and mRNA regulatory network in EGFR-mutated lung adenocarcinoma [miRNA]

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

MicroRNA and mRNA regulatory network in EGFR-mutated lung adenocarcinoma [mRNA]

2018-11-13 | GSE119267 | GEO

Specific expression of MUC21 in micropapillary elements of lung adenocarcinomas - Implications for the progression of EGFR-mutated lung adenocarcinomas.

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Discovery of somatic mutations in lung adenocarcinomas

Project description:This was a collaborative study to discover somatic mutations in 188 lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are likely to play a role in carcinogenesis. The observed mutational profiles correlate with clinical features, smoking status, and DNA repair defects. These results are complemented by data integration including SNP array data and gene expression array data (deposited here). Our findings shed further light on several key signaling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.

2008-09-05 | GSE12667 | GEO

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