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Whole transcriptome analysis of erlotinib treatment in EGFR-mutant cells

ABSTRACT: We were interested in characterizing the transcriptional changes that occur on a genome-wide scale following treatment of EGFR-mutant lung cancer cells with targeted therapies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51212 | GEO | 2015/02/25

SECONDARY ACCESSION(S): PRJNA221626

REPOSITORIES: GEO

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Whole transcriptome analysis of erlotinib treatment in EGFR-mutant cells

Project description:We were interested in characterizing the transcriptional changes that occur on a genome-wide scale following treatment of EGFR-mutant lung cancer cells with targeted therapies. HCC827 human lung cancer cells harboring an amplified EGFR allele with an activating in frame deletion of 15 nucleotides in exon 19 were treated in triplicate with 1uM erlotinib (EGFR inhibitor), AZD-6244 (MEK inhibitor) or BEZ-235 (PI3-Kinase/mTOR inhibitor) for 6 hours, followed by total mRNA isolation and whole transcriptome analysis using Affymetrix U133 Plus 2.0 expression arrays.

2015-02-25 | E-GEOD-51212 | biostudies-arrayexpress

Expression data from EGFR WT or EGFR mutant NSCLC with or without erlotinib

Project description:Non-small cell lung cancers (NSCLCs) harboring activating EGFR mutants show dramatic responses to EGFR TKIs, such as erlotinib and geffitinib. However, nearly all patients show relapse within 1 year after initial treatment. We used microarrays to detail global gene expression changes in EGFR mutant cells vs. WT cells responding to erlotinib. 4 EGFR mutant and 4 WT NSCLC cells were treated with or without erlotinib for 24 hr, followed by RNA extraction and hybridization on Affymetrix microarrays.

2014-05-16 | E-GEOD-57156 | biostudies-arrayexpress

Expression data from EGFR WT or EGFR mutant NSCLC with or without erlotinib

2014-05-16 | GSE57156 | GEO

Whole transcriptome analysis of erlotinib treatment in EGFR-mutant cells

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Angiogenin/ribonuclease 5 is an EGFR ligand and a serum biomarker for erlotinib sensitivity in pancreatic cancer

Project description:Pancreatic ribonuclease (RNase) is a secreted enzyme critical for host defense. We discover an intrinsic RNase function, serving as a ligand for epidermal growth factor receptor (EGFR), a member of receptor tyrosine kinase (RTK), in pancreatic ductal adenocarcinoma (PDAC). The closely related bovine RNase A and human RNase 5 (angiogenin/ANG) can trigger oncogenic transformation independently of their catalytic activities via direct association with EGFR. Notably, high plasma ANG level in PDAC patients is positively associated with response to EGFR inhibitor erlotinib treatment. These results identify a previously unrecognized role of ANG as a serum biomarker, which may be used to stratify patients for EGFR-targeted therapies, and offer insights into the ligand-receptor relationship between RNase and RTK families.

2018-04-18 | GSE109427 | GEO

Intermittent high-dose treatment with erlotinib enhances therapeutic efficacy in EGFR-mutant lung cancer.

Project description:Treatment with EGFR kinase inhibitors improves progression-free survival of patients with EGFR-mutant lung cancer. However, all patients with initial response will eventually acquire resistance and die from tumor recurrence. We found that intermittent high-dose treatment with erlotinib induced apoptosis more potently and improved tumor shrinkage significantly than the established low doses. In mice carrying EGFR-mutant xenografts intermittent high-dose treatment (200 mg/kg every other day) was tolerable and prolonged progression-free survival and reduced the frequency of acquired resistance. Intermittent EGFR-targeted high-dose schedules induce more profound as well as sustained target inhibition and may afford enhanced therapeutic efficacy.

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TRANSCRIPTIONAL EFFECTS OF INHIBITING EGFR IN KERATINOCYTES

Project description:EGFR activation is important in human epithelial malignancies, including cutaneous squamous cell carcinoma, lung, colon, pancreatic and other cancers. Therapies targeting EGFR are currently used to treat such cancers, but one significant drawback to EGFR inhibitor therapies is the associated skin toxicity. This toxicity usually presents as papular or pustular folliculitis, dry skin with pruritus and hair and nails abnormalities. The side effects often limit the usefulness of EGFR inhibitors in cancer treatment. The transcriptional changes caused by EGFR inhibition in epidermal keratinocytes have not been extensively explored. To define the transcriptional changes caused by inhibition of EGFR in primary human epidermal keratinocytes, we treated these cells with Tyrphostin and compared treated and control cultures in parallel, using Affymetrix microarrays. Using metaanalysis approaches, we integrated the observed changes with a large set of already existing data on transcriptional profiling in epidermal keratinocytes. We found that EGFR inhibition suppresses expression of genes associated with keratinocyte proliferation, attachment and motility. Apoptosis is facilitated by both induction of proapoptotic and suppression of antiapoptotic genes. Surprisingly, EGFR inhibition induces expression of markers of epidermal differentiation. Time course of human epidermal keratinocytes treated with Tyrphostin (AG1478) and untreated controls

2012-10-19 | E-GEOD-41680 | biostudies-arrayexpress

The gene expression profiles of EGFR-mutant SCLC cell lines derived from lung adenocarcinoma patients after failed EGFR-TKI treatment.

Project description:In this study, we established 2 EGFR-mutant SCLC cell lines from lung adenocarcinoma patients after failed EGFR-TKI treatment. These 2 EGFR-mutant SCLC cell lines displayed 2 different phenotypes: suspensive and adherent. We used microarrays to identify the global gene alterations and molecular basis of EGFR-mutant SCLC cell lines.

2018-11-20 | GSE122698 | GEO

Expression comparison of mutant EGFR-driven gliomas with relapse tumors upon mutant EGFR ablation

Project description:To determine the roles of oncogenic EGFR signaling in gliomagenesis and tumor maintenance, we generated a novel glioma mouse model driven by inducible expression of a mutant EGFR (EGFR*). Genetic suppression of EGFR* induction led to significant tumor regression and prolonged survival. But in spite of the initial response, the tumors relapsed invariably and propagated independent of EGFR*. We used microarrys to directly compare geen expression of control and relapse tumors and identified gene sets specifically activated in relapse tumors. Control and relasped glioma samples upon mutant EGFR extinction were selected for RNA extraction and hybridization on Affymetrix microarrays.

2015-01-08 | E-GEOD-64751 | biostudies-arrayexpress

Expression comparison of mutant EGFR-driven gliomas with relapse tumors upon mutant EGFR ablation

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