E-GEOD-4066
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA95191
PROVIDER: E-GEOD-4066 | ExpressionAtlas | 2014-10-10
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-4066-analysis-methods.tsv | Tabular | |||
| E-GEOD-4066-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-4066-configuration.xml | Xml | |||
| E-GEOD-4066-percentile-ranks.tsv | Tabular | |||
| E-GEOD-4066.condensed-sdrf.tsv | Tabular |
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Project description:Peripheral blood lymphocytes from a total of 57 patients were immortalized with Epstein-Barr virus. Fourteen radiation-therapy patients suffered unusual levels of radiation toxicity (RadS). Thirteen radiation-therapy patients with limited toxicity (RadC) were enrolled as controls. Fifteen patients diagnosed with skin cancer before age 40 (SkCa) were used as a second group of controls. Fifteen healthy subjects without any history of cancer (NoCa) were matched to the skin cancer patients and used as a third group of controls. Cells were exposed to mock treatment (Mock), ultra-violet radiation (UV), or ionizing radiation (IR). For UV radiation treatment, cells were exposed to 10 J/m^2 and harvested for RNA 24 hours later. For IR treatment, cells were exposed to 5 Gy of IR and harvested for RNA 4 hours later. For example, RadS1-Mock refers to cells from radiation sensitive patient 1 exposed to mock treatment. The published manuscript (PNAS 101:6634, 2004) can be found at http://www.pnas.org/cgi/doi/10.1073/pnas.0307761101; Data were analyzed with Affymetrix MAS version 4.0. Normalization â?? A reference data set was generated by averaging the expression of each gene over all data sets. The data for each hybridization were compared with the reference data set in a cube root scatter plot. A linear least-squares fit to the cube root scatter plot was then used to normalize each hybridization.
2007-08-05 | E-GEOD-1725 | biostudies-arrayexpress
Project description:Peripheral blood lymphocytes from a total of 57 patients were immortalized with Epstein-Barr virus. Fourteen radiation-therapy patients suffered unusual levels of radiation toxicity (RadS). Thirteen radiation-therapy patients with limited toxicity (RadC) were enrolled as controls. Fifteen patients diagnosed with skin cancer before age 40 (SkCa) were used as a second group of controls. Fifteen healthy subjects without any history of cancer (NoCa) were matched to the skin cancer patients and used as a third group of controls. Cells were exposed to mock treatment (Mock), ultra-violet radiation (UV), or ionizing radiation (IR). For UV radiation treatment, cells were exposed to 10 J/m^2 and harvested for RNA 24 hours later. For IR treatment, cells were exposed to 5 Gy of IR and harvested for RNA 4 hours later. For example, RadS1-Mock refers to cells from radiation sensitive patient 1 exposed to mock treatment. The published manuscript (PNAS 101:6634, 2004) can be found at http://www.pnas.org/cgi/doi/10.1073/pnas.0307761101 Data were analyzed with Affymetrix MAS version 4.0. Normalization – A reference data set was generated by averaging the expression of each gene over all data sets. The data for each hybridization were compared with the reference data set in a cube root scatter plot. A linear least-squares fit to the cube root scatter plot was then used to normalize each hybridization. Keywords = Gene expression in lymphoid cells of cancer patients Keywords: repeat sample
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Project description:Exposure to ultraviolet (UV) irradiation is the major cause of nonmelanoma skin cancer, the most common form of cancer in the United States. UV irradiation has a variety of effects on the skin associated with carcinogenesis, including DNA damage and effects on signal transduction. The alterations in signaling caused by UV regulate inflammation, cell proliferation, and apoptosis. UV also activates the orphan receptor tyrosine kinase and proto-oncogene Erbb2 (HER2/neu). In this study, we demonstrate that the UV-induced activation of Erbb2 regulates the response of the skin to UV. Inhibition or knockdown of Erbb2 before UV irradiation suppressed cell proliferation, cell survival, and inflammation after UV. In addition, Erbb2 was necessary for the UV-induced expression of numerous proinflammatory genes that are regulated by the transcription factors nuclear factor-kappaB and Comp1, including interleukin-1beta, prostaglandin-endoperoxidase synthase 2 (Cyclooxygenase-2), and multiple chemokines. These results reveal the influence of Erbb2 on the UV response and suggest a role for Erbb2 in UV-induced pathologies such as skin cancer. Keywords: time course, ultraviolet irradiation, UV, erbB2, mouse skin The dorsal skin of adult female CD-1 mice was clipped one day before treatment and shaved on the day of treatment. DMSO or 4 mg AG825 dissolved in DMSO was applied topically to the shaved back of the mice 2 h prior to exposure to 10 kJ/m^2 UV or sham irradiation. The UV dose was approximately 30% UVA, 70% UVB and <1% UVC, with a total output of 470 uW/cm^2. Flash frozen skin was removed and total RNA expracted with TRIzol reagent (Invitrogen) and further purified with an RNeasy kit (Qiagen). Amplification, reverse-transcription, biotinylation, and hybridization were all carried out under standard conditions and procedures recommended by the manufacturer.
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