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Molecular mechanisms and potential therapeutic drugs linking to cetuximab-induced reactions in human cells (HaCaT cells)

ABSTRACT: Molecular mechanisms and potential therapeutic drugs linking to cetuximab-induced reactions in human cells (HaCaT cells)

PROVIDER: PRJNA438485 | ENA |

REPOSITORIES: ENA

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Molecular mechanisms and potential therapeutic drugs linking to cetuximab-induced reactions in human cells (HaCaT cells)

Project description:To obtain differentially expressed genes associated with cetuximab induced cytotoxicity we analyzed RNA samples using whole genome microarray expression profiling as a discovery platform to identify genes . Two kinds of RNA samples were extracted from HaCaT and HEK 293 cell; without cetuximab and incubation for 24 hours with 1.63μM (fixed maintenance dose) cetuximab.

2018-09-30 | GSE111885 | GEO

Molecular mechanisms and potential therapeutic drugs linking to cetuximab-induced reactions in human cells

Project description:Molecular mechanisms and potential therapeutic drugs linking to cetuximab-induced reactions in human cells

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Molecular mechanisms and potential therapeutic drugs linking to cetuximab-resistance reactions in cancer cells

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Molecular mechanisms and potential therapeutic drugs linking to cetuximab-induced reactions in human cells (HEK 293 cells)

2018-09-30 | GSE111886 | GEO

Molecular mechanisms and potential therapeutic drugs linking to cetuximab-induced reactions in human cells (HEK 293 cells)

Project description:Molecular mechanisms and potential therapeutic drugs linking to cetuximab-induced reactions in human cells (HEK 293 cells)

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Molecular mechanisms and potential therapeutic drugs linking to cetuximab-resistance reactions in cancer cells

Project description:To obtain differentially expressed genes associated with cetuximab resistance mechanism, we analyzed RNA samples using whole genome microarray expression profiling as a discovery platform to identify genes. Two kinds of RNA samples were extracted from SAS, Sa3, and HSC-3 cells: control cells and cetuximab-resistant cells.

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Molecular mechanisms and potential therapeutic drugs linking to cetuximab-induced reactions in human cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-09-30 | GSE111887 | GEO

Gene expression signatures modulated by epidermal growth factor receptor activation and their relationship to cetuximab resistance in head and neck squamous cell carcinoma

Project description:Aberrant activation of signaling pathways controlled in normal epithelial cells by the epidermal growth factor receptor (EGFR) has been linked to cetuximab (a monoclonal antibody against EGFR) resistance in head and neck squamous cell carcinoma (HNSCC). To infer relevant and specific pathway activation downstream of EGFR from gene expression in HNSCC, we generated gene expression signatures using immortalized keratinocytes (HaCaT) subjected to either ligand stimulation or pharmacological inhibition of the signaling intermediaries PI-3-Kinase and MEK or transfected with EGFR, RELA/p65, or HRASVal12. The gene expression patterns that distinguished the various HaCaT variants and conditions were inferred using the Markov chain Monte Carlo (MCMC) matrix factorization algorithm Coordinated Gene Activity in Pattern Sets (CoGAPS). This approach inferred gene expression signatures with greater relevance to cell signaling pathway activation than the expression signatures inferred with standard linear models. Furthermore, the pathway signature generated using HaCaT-HRASVal12 further associated with the cetuximab treatment response in isogenic cetuximab-sensitive (UMSCC1) and -resistant (1CC8) cell lines. Our data suggest that the CoGAPS algorithm can generate gene expression signatures that are pertinent to downstream effects of receptor signaling pathway activation and potentially be useful in modeling resistance mechanisms to targeted therapies. 58 total RNA collected from HaCaT cell lines with combinations of the following experimental conditions: forced expression of EGFR, RELA/p65, and HRAS-VAL12D; grown in PBS, serum starve, and media stimulated with TNF or EGF; treated with gefitinib, LY294002, and U1026.

2012-05-22 | E-GEOD-32975 | biostudies-arrayexpress

Gene expression signatures modulated by epidermal growth factor receptor activation and their relationship to cetuximab resistance in head and neck squamous cell carcinoma

2012-05-23 | GSE32975 | GEO

Global gene expression analysis between cetuximab-sensitive and cetuximab-resistant colorectal cancer cells

Project description:Cetuximab is an epidermal growth factor receptor (EGFR)-blocking antibody approved for treatment of metastatic colorectal cancer. We examined differences in global gene expression between the syngeneic DiFi colorectal cancer cells, and a subline of DiFi cells with acquired resistance to cetuximab (DiFi5). We used Affymetrix HG-U133A array to compare the expression pattern of genes that are up-regulated or down-regulated between the parental DiFi colorectal cancer cells and the cetuximab-resistant DiFi5 cells. We generated a cetuximab-resistant DiFi subline, termed DiFi5, by chronic exposure of parental DiFi cells to serially increased doses of cetuximab (from 0.5 nM to 5 nM) for over 1 year. The resulting DiFi5 subline exhibits significant resistance to cetuximab-induced apoptosis. After we confirmed that the phenotype was stable over a period of time of more than 6 months, the RNA from DiFi and DiFi5 cells were extracted and hybridized to an Affymetrix HG-U133A array according to the manufacturerâs instructions. Following the hybridization, the array was scanned using a laser confocal scanner, and microarray image data were analyzed using DNA-Chip Analyzer (dChip), version 1.3, by the Sequencing and Microarray Facility at MD Anderson Cancer Center.

2016-07-17 | E-GEOD-71210 | biostudies-arrayexpress

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